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Sympathomimetics (Adrenergic Agonists)—Epinephrine, Norepinephrine - Alpha & Beta Receptors

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hello wonderful people it's medicosa's

perfect snail is where medicine makes

perfect sense welcome back to my

pharmacology playlist in previous videos

we talked about the arachidonic acid

pathway medications to treat asthma and

COPD Heparin Warfarin anti-platelets

thrombolytics and even anti-seizure

medications as for today we shall talk

about sympathomimetics the drugs that

mimic the sympathetic nervous system and

since sympathetic fiber secretes nor

adrenaline therefore the

sympathomimetics are Agnes on adrenergic

receptors adrenergic from adrenaline or

noradrenaline if the parasympathetic

nervous system was about nicotinic and

muscarinic receptors then the

sympathetic nervous system is all about

Alpha receptors and beta receptors today

we'll talk about Alpha and Beta agonists

And in the next video we'll talk about

sympatholytics or adrenergic antagonists

now click the like button click the

Subscribe button and let's get started

this video was made possible through the

generous support of Maria so please take

a moment to say thank you to Maria in

the comments remember that the autonomic

nervous system has three parts

parasympathetic nervous system

sympathetic nervous system and enteric

nervous system parasympathetic is all

about rest and digest but sympathetic is

about what it's about fight flight so to

understand the functions of the

sympathetic autonomic nervous system

just imagine yourself for running from a

tiger quick neuro review remember when

we divided the brain through an

imaginary line in the sand in front his

motor behind a sensory the same fact

applies to the spinal cord in front is

motor behind its sensory how about the

autonomic nervous system well if I have

a sensory fiber sensory autonomic fiber

it's going to enter through the afferent

which is posterior behind the line

because it's censoring but if I have

something to move the gland to secrete

for example or constrict a vessel then

these fibers will originate from the

lateral horn cell in front of the line

because this will be an autonomic motor

fiber the sympathetic nervous system is

fight flight the parasympathetic nervous

system is rest and digest I.E Secreto

motor sympathetic nervous system is

thoracolumbore but the parasympathetic

nervous system is craniosacral the

post-ganglionic sympathetic fibers

secrete nor adrenaline but the

parasympathetic fiber secretes

acetylcholine since noradrenaline is

here we call this adrenergic fibers

since we have acetylcholine there we

call the parasympathetic cholinergic

fibers who's going to be waiting for the

adrenergic chemicals adrenergic

receptors such as Alpha receptors and

beta receptors but who's waiting for the

cholinergic fibers who's waiting for the

acetylcholine cholinergic receptors I

mean nicotinic and muscarinic so the

origin of the sympathetic nervous system

is thoracolumbore and from there they

reach the rest of your body after

relaying in ganglia so I will have a

lovely fiber here starting in the spinal

cord and then reaching the ganglion

another neuron will start in the

ganglion until I reach the target organ

let's say your heart the effects of the

sympathetic autonomic nervous system

were discussed before in my physiology

playlist let's review them quickly

imagine that I am running from a tiger

fight flight what's going to happen to

my pupil dilates what's going to happen

to my eyelid elevates skin I have

vasoconstriction of the vessels of the

skin will I secrete some sweat of course

what's going to happen in my thorax when

it comes to my bronchi they will dilate

because I'm running from a tiger so I

need to breathe more by the same token I

need to see better the danger in front

of me and the danger behind me for that

matter as for the heart sympathetic

nervous system will boost a heart rate

stroke volume which means contractility

I.E it is a positive inotropic

chronotropic dromotropic best meotropic

Etc all of the effects on the heart

happen because of beta 1 receptor

stimulation but dilation of my bronchi

happens thanks to Beta 2 stimulation how

do I remember it well you have one heart

but two lungs so beta 1 is in the heart

beta 2 is in the lung a better way to

remember them is by their importance

imagine that you are a scientist and you

have a receptor on the Heart Another

receptor on the lungs which one takes

priority the heart of course so beta 1

is in the heart beta 2 is in the lungs

as well as other places and the abdomen

when I'm running from a tiger I need

metabolism so please secrete that

epinephrine or epineph from my Adrenal

medulla and these will do what well what

does epinephrine do epinephrine is

anti-insulin insulin was anabolic but

epinephrine is catabolic let's break

down your glycogen to glucose to give

you energy to run let's break down the

triglycerides into free fatty acids I.E

lipolysis and since epinephrine is

anti-insulin epinephrine will reduce

insulin secretion but will boost

glucagon secretion a very important

Point indeed because this is all about

the most important dichotomy in medicine

or distinction feeding State versus

fasting State when you're running from a

tiger you're in the fasting State you're

not eating while running from a tiger

you're not in the anabolic land but in

the catabolic land you're not in the

land of abundance but in the land of

scarcity you are not in the insulin

World instead you are in the glucagon

world the insulin World I.E feeding

state is anabolic it's a builder it

builds up amino acids into bigger

proteins and builds up the small glucose

into bigger glycogen and builds up the

free fatty acids into bigger

triglycerides they is in the land of

feeding but when I'm running from a

tiger I am in the land of scarcity in

the land of fasting so it's not insulin

this time but glucagon and not just

glucagon glucagon and his friends who

are his friends epinephrine is one of

them cortisol is another one of them and

freaking thyroxine is another one of

them all of them are catabolic hormones

for the most part so when I'm running

from a tiger this is sympathetic which

means my Adrenal medulla will secrete

epinephrine which means epinephrine will

break down glycogen into glucose hashtag

glycogenolysis it will break down

triglycerides into free fatty acids

which is lipolysis and if you keep

running for days it will break down your

proteins into amino acids take those

amino acids and try to convert them to

glucose especially the glycogenic amino

acids hashtag

gluconeogenesis Genesis formation of

glucose from new sources what else

happened when I ran from a tiger well

what are the two most important organs

in your body heart and brain of course

or brain and heart amazing so I will

boost the blood supply to your brain and

your heart but what else do you need in

order to run from a tiger I need my

skeletal muscles so I will shunt the

blood away from the organs that you do

not need right now such as the skin and

the gastrointestinal tract because we do

not have enough time to rest and digest

poop and pee in this time and instead we

shift that valuable blood to your brain

your heart and your skeletal muscles

which means we will constrict the blood

vessels in your skin and

gastrointestinal system but we'll do the

opposite we will dilate the blood

vessels in your brain heart and skeletal

muscles especially the heart and

skeletal muscles how do you constrict

these vessels Alpha One receptor

stimulation how do you dilate other

vessels beta 2 receptor stimulation and

that's why you need different types of

receptors cause the same freaking

epinephrine can lead to vasoconstriction

on some receptors and vasodilation on

other receptors even though it is the

same chemical that's why you need

receptors something that your great

Professor will never tell you the same

concept applies to the bladder the

sympathetic nervous system dilates my

urinary bladder because I do not have

time to urinate when I'm running from a

tiger it'll be embarrassing to say the

least if not time consuming and

life-threatening so I will dilate the

bladder wall amazing and then what

what's going to happen after you dilute

the bladder wall I will do the opposite

to the sphincter I will constrict my

urethral sphincter oh how do you dilate

something and constrict something well

because the bladder has beta receptors

but the sphincters have Alpha receptor

oh I get it see medicine makes so much

sense once you understand what the

french toast you're talking about

remember that the output of the heart or

cardiac output equals to how fast the

heart is pumping times how strong the

heart is pumping heart rate means how

many beats per minute stroke volume

means how much volume per stroke when

you multiply them together you get how

much volume pumped by the heart in one

minute and if you take that lovely

cardiac output put it here multiply it

by the total peripheral resistance also

known as the systemic vascular

resistance what do you get I get the

main systemic arterial blood pressure

today we're talking about

sympathomimetics some of them will

increase heart rate and or stroke volume

and what's going to happen when you

increase heart rate and stroke volume

you increase the cardiac output and when

the cardiac output goes up what's going

to happen to blood pressure it also

increases how did I erase the heart rate

and the stroke volume remember that the

beta 1 is on the heart oh so beta 1

stimulation raise the stroke volume and

and the heart rate and therefore the

cardiac output and therefore the blood

pressure also alpha 1 stimulation will

do what it will constrict my vessels and

when you constrict the vessels what's

going to happen to the radius the radius

decreases so what's going to happen to

the resistance resistance increases

including the total peripheral

resistance and when the resistance goes

up what's going to happen to the blood

pressure it too shall increase so here's

cardiac output it equals heart rate time

stroke volume how fast times how strong

for example if the heart rate is 100

beats per minute and the stroke volume

is 50 ml per bit you can just multiply

this by this and we can cancel beat

upstairs with bait downstairs we get the

cardiac output in MLS per minute the

blood pressure or the mean systemic

arterial blood pressure to be specific

equals cardiac output times total

peripheral resistance beta when agonists

increase heart rate and stroke volume

therefore increase cardiac output and

blood pressure and Alpha One agonists

increase tpr also increasing blood

pressure remember that Alpha One

constrict vessel when I constrict

vessels or radius goes down but

resistance goes up resistance goes up

meaning total peripheral resistance went

up you can think of it also as the blood

pressure equals force over area as I

constrict The Vessel the surface area

decreases so the blood pressure

increases if I am talking about a

sympathetic fiber I'm talking about the

post-ganglionic sympathetic but before

the posting ionic we had a ganglion and

we had what we had preganglionic where

did we start it's thoracolumbar so I

started at the lateral horn cell in the

thoraco OR lumbar region then I have

pre-ganglionic fiber which by the way

secretes acetylcholine we call these

pre-ganglionic since they secrete

acetylcholine they are cholinergic

what's the name of the acetylcholine

receptor waiting on the ganglion that's

nicotinic sub n then we have the

ganglion and post-ganglionic fibers that

are adrenergic because they secrete nor

adrenaline onto Alpha and beta receptors

cholinergic fibers are nicotinic or

muscarinic but adrenergic fibers or

alpha or beta here is an adrenergic

fiber look at this norepinephrine

postganglionic sympathetic and then

after norepinephrine gets released into

the synaptic cleft it can act on alpha-1

or beta1 but look here we have

acetylcholine from a cholinergic

receptor such as the post-ganglionic

parasympathetic fibers secreting

acetylcholine because they are

cholineergic acetylcholine can act on

nicotinic receptors or muscarinic

receptors since today's video is talking

about sympathomimetics we will focus on

Alpha and beta receptors what do

sympathetic fibers secrete they can

secrete norepinephrine but not

epinephrine who secretes epinephrine

then only the Adrenal medulla because as

the Adrian medulla goes this way

phenylalanine and tyrosine doped

dopamine norepinephrine epinephrine or

phenylalanine tyrosine dopedopamine nor

adrenaline adrenaline their dream

medulla can go all the way until we get

epinephrine out however if this was a

sympathetic nerve fiber it can only

secrete norepinephrine but it cannot

secrete epinephrine why not because it

lacks the final enzyme which is known as

phenyl ethanolamine and methyl

transferase only the Adrenal medulla

possess such an enzyme here is the

sympathetic nerve fiber phenylene

tyrosine dopedopamine and then

norepinephrine there is no epinephrine

here nor epinephrine will leave their

presynaptic neuron it will go to the

synapse it has options such as acting on

the alpha-1 receptor on the Alpha 2

receptor beta 1 or beta 2. let me tell

you something Alpha 2 is

anti-sympathetic how do I remember it

Alpha 2 with a 2 with a t is n tie

sympathetic and what do I mean by that

if you stimulate the Alpha 2 receptor it

will inhibit the release of

norepinephrine from the presynaptic

neuron back to norepinephrine in the

synapse it can act on Alpha 1 Alpha 2

beta 1 or beta 2 or even beta3 after it

has performed its function it's time to

get rid of it we can degrade it by comt

enzyme which stands for catecholamine o

methyl transferase because

norepinephrine is one of the

catecholamines and this breaks down or

epinephrine into some metabolites that

can get excreted by the kidney or

besides breaking it down we can reuptake

it back into the presynaptic neuron

who's going to take care of it here the

Mao enzyme monoamine oxidase we can also

recycle it back into the vessel please

note the comt exists in the synapse

however Mao enzyme exists in the

presynaptic nerve terminal Alpha 2 is

anti-sympathetic right but have heard

Alpha One no Alpha 1A is the sympathetic

what does it do well Alpha One is a hero

of constriction of vessels contraction

of the dilator pipeli muscle to cause

midoriasis or dilation of the pupil

stimulation of alpha 1 constricts the

sphincters of the GI tract and the

geotract gastrointestinal and genital

urinary look I'm closing the sphincters

by stimulating alpha-1 nor epinephrine

for example is an alpha one Agonist

which means it simulates Alpha and

receptors how about phentolamine and

phenoxybenzamine they are antagonists

they block the alpha-1 receptor so we're

done with the alphas alpha-1 constricts

vessels dilates pupils Alpha 2 is

anti-sympathetic by preventing the

release of norepinephrine from the

synaptic vesicle but how about the betas

betas for the most part are inhibitory

on everything you can imagine except

three things on the heart on hormones

and Metabolism because beta 1 stimulates

the heart it increases heart rate stroke

volume contractility its positive

inotropic chronotropic dromotropic Etc

it is stimulatory on hormones such as

hormones of metabolism example lipolysis

but everything else beta is inhibitory

it inhibits the contraction of by

bronchi so my bronchi dilate it inhibits

the contraction of gastric muscles and

the smooth muscles of gastrointestinal

and genital urinary so they relax beta

is inhibitory it relaxes the uterus wall

can you give me examples of a beta

Agonist epinephrine epinephrine is an

Agonist on beta as well as Alpha how

about a Blocker of the beta receptors an

antagonist any drug that ends in Olo

such as Propranolol metoprolol

ete nolol Etc Alpha One receptors are GQ

coupled anytime you hear of G Q think of

calcium which is the hero of contraction

of smooth muscle as for Alpha 2 it is

anti-sympathetic what do you mean by

anti it is inhibitory GI for inhibitory

as for all the betas they are GS coupled

and if something is GS coupled it will

raise the cyclic amp what happens when I

run from a tiger glycogen gets broken

down to glucose Alpha One can help me

with this glycogenolysis I break down

triglycerides into free fatty acids beta

especially beta 3 can help me with this

process I'm gonna dilate my bronchi

which will help me breathe I'm going to

increase all of my cardiac properties so

that I can provide my body with energy

while running from a tiger the

sympathetic nervous system constricts

almost all of the vessels except the

vessels going to your skeletal muscles

the vessels going to your heart what

does alpha one do alpha 1 constricts

remember Alpha One is GQ coupled and GQ

means calcium which is the hero of

contraction of smooth muscles so I'm

gonna to contract the smooth muscles in

the pupil especially the dilator P belly

muscle to dilate the pupil I'm gonna

contract the smooth muscles in the

vessels and by vessels I mean arteries

and veins when I constrict those

arterials I raise the afterload which

raises the diastolic blood pressure when

I constrict those arterials I raise the

total peripheral resistance or systemic

vascular resistance so overall the mean

systemic blood pressure goes up how

about constricting veins when I

constrict veins I increase the venous

return back to the heart this is the

right side of the heart I have right

atrium here right ventricle there and I

have left atrium here left ventricle

there remember that the right atrium is

connected to superior vena cava and

inferior vena cava by constricting veins

what's going to happen you're increasing

the venous return because you're

squeezing them into the right atrium and

this increases venous return which

increases preload which increases

systolic blood pressure because when

there is more input to the hot there

will be more output from the heart

stroke volume goes up and cardiac output

goes up anytime you constrict veins

what's going to happen to the

capacitance of the vein well the

capacitance decreases because I'm

constricting them and they are emptying

their blood into the right atrium Alpha

One stimulation tends to reduce renin

release from the kidney conversely beta

1 stimulation tends to boost Ren and

release Alpha One decreases running

release but beta 1 stimulation raises

run and release so what does renin do

renin is a hormone secreted by the kid

it's also an enzyme that converts

angiogen Cyanogen to Angiotensin one

Angiotensin 1 will be converted to

angiogen sin 2 thanks to Ace enzyme in

the lungs usually Angiotensin II has two

functions function number one to

vasoconstrict the arterials and raise

the blood pressure function number two

is to tell the zone agglomerulosa of the

adrenal cortex X to make aldosterone

aldosterone will reabsorb two things and

secrete two things it will reabsorb

sodium and water but secrete potassium

and hydrogen when you reabsorb sodium

and water you're more likely to raise

the blood pressure so Angiotensin II had

two functions to constrict the

arterioles which raises blood pressure

and to secrete aldosterone which also

can raise the blood pressure why do you

call tangutansin because I tense the

angio I constrict the vessels Alpha One

tends to decrease renin but beta 1 tends

to increase renin how about Alpha 2

Alpha 2 is anti-sympathetic which means

if you stimulate this presynaptic Alpha

2 what's going to happen you will

release less norepinephrine to the

synapse remember that the sympathetic

nervous system is fight flight this is

the adrenergic system it's the land of

epinephrine or epinephrine don't forget

that epinephrine which is catabolic is

anti-insulin which is anabolic which

makes sense sense because Alpha 2

stimulation decreases insulin release

from the pancreas so we talked about

alpha 1 and Alpha 2. let's talk about

the betas beta 1 remember your heart it

increases all of the cardiac properties

positive chronotropic inotropic

dromotropic by chronotropic I mean it

increases heart rate by positive

inotropic I mean it increases

contractility when you contract harder

you pump out more volume so stroke

volume goes up when stroke volume goes

up cardiac output goes up when cardiac

output goes up this is solid blood

pressure goes up beta 1 also increases

running release from the kidney beta 1

increases aqueous humor secretion in the

eye and how about beta 2 remember you

have two lungs okay so it's going to

dilate the bronchi beta 2 is inhibitory

it relaxes muscle it relaxes the smooth

muscles in my bronchi it relaxes the

smooth muscles of the uterus and this is

called a tocolytic effect Toco means

contraction lysis means breakdown down

when you break down contractions you're

causing relaxation when I evasive dilate

what's going to happen to the radius of

the vessel it increases which means

what's going to happen to the resistance

it decreases so the afterload goes down

and the diastolic blood pressure tends

to decrease and the overall mean

systemic blood pressure tends to

decrease beta 2 do something important

which is they boost the uptake of

potassium into the muscle so here is the

muscle and this is the blood vessel

under beta 2 stimulation the potassium

will leave the blood and go into the

cell such as the muscle cell too much

beta 2 stimulation can lead to

hypokalemia beta 2 is important also for

metabolism such as

gluconeogenesis and glycogenolysis how

about beta 3 oh that's the land of

lipolysis break down the triglycerides

into free fatty acids and cholesterol

and beta 3 is also present in the

urinary bladder arguably it relaxes the

wall of the bladder there is something

important that we need to mention which

which is the better receptor reflex

let's suppose that for whatever reason

my blood pressure drops when my blood

pressure drops the baroreceptors which

are the receptors that sense that change

in pressure will sense the hypotension

and they will tell the brain hey brain

we have a disaster outside there is low

blood pressure so the brain will sense

the danger and will send the sympathetic

its fight flight it's a dangerous

situation they have hypotension so I

send sympathetic fibers to do what to

release norepinephrine from the nerve

fibers what does norepinephrine do to

the heart it stimulates beta 1 and when

you stimulate beta 1 what's going to

happen to heart rate it increases stroke

volume also increases that's it to your

only stimulating beta1 no as nor

epinephrine I can also stimulate alpha

one so I constrict veins and arteries

when I constrict veins I increase venous

return to the heart and when I constrict

arterials I increase the systemic blood

pressure so by increasing heart rate and

contractility and increasing venous

return and increasing systemic blood

pressure I am trying to raise the blood

pressure back to normal so the moral of

the story is hypotension usually causes reflex

reflex

tachycardia conversely what if I start

with hypertension the opposite will

happen the brain will sense the high

pressure and will send the opposite it

will send parasympathetic the vagus

nerve to do what to do the opposite I

want to decrease heart rate and decrease

contractility so that I can bring the

blood pressure down and back to normal

so the moral of the story is

hypertension can lead to reflex

bradycardia so hypotension causes reflex

tachycardia but hypertension causes

reflex bradycardia it's the land of

opposites so what are these adrenergic

agonists or sympathomimetics which are

the topic of today's video remember that

we have Alpha One Alpha 2 beta 1 and

beta 2. the alpha-1 agonists include

phenylephrine Alpha 2 agonists include

clonidine and Alpha methyl dopa how

about a beta-1 Agonist I can say

isoproterinol knowing that isoproternal

is beta 1 and beta 2 Agonist beta 2

agonists include albuterol salbutamol

turbitaline then we have mixed agonists

which mean they are agonists on Alpha

and beta and they include epinephrine or

epinephrine dopamine collectively known

as the catecholamines and speaking of

dopamine we have something called the D1

receptor phenoldopam is a medication

that is D1 Agonist and here is another

classification the adrenergic Agonist or

sympathomimetics include the endogenous

natural catecholamines epinephrine or

epinephrine and dopamine how about

catecholamines that are not made in the

body synthetic catecholamines include

isopropterino and dobutamine then we

have a synthetic

non-katecholamines we have direct acting

and indirect acting direct acting

synthetic non-catecholamines include

phenylephrine methoxamine Albuterol

terbitaline and for Alpha 2 we have

clonidine and Alpha methyl dopa I put

them together here because they are

alpha two and because Alpha 2 is

anti-sympathetic indirect acting meaning

they will boost the availability of

norepinephrine in the synaptic cleft

they include ephedrine amphetamine

methinteramine metaraminol cocaine and

tricyclic antidepressants here is my

pre-synaptic terminal containing

norepinephrine here's the synaptic cleft

and here's the postsynaptic neuron what

do we have here norepinephrine making

this an adrenergic fiber look at my

adrenergic fiber amazing now what I can

block the transport into the vesicle

such as a reservine if I cannot put

norepinephrine into the vesicle I cannot

release norepinephrine from the vesicle

later how about I boost the release of

norepinephrine IE I'm a relator that's

the story of amphetamines tyramine and

ephedrine how about inhibiting the

release which is the opposite of

releaser release Inhibitors include

goanthidine and britillion then

norepinephrine is secreted it can act on

alpha-1 which is GQ coupled meaning it's

going to increase the calcium and

contract smooth muscles or

norepinephrine can act on beta receptors

they are GS coupled and they will raise

the cyclic amp so we have Alpha agonists

and alpha blockers we have beta agonists

and beta blockers after norepinephrine

has performed this function now what now

it will be degraded by comt we have comt

Inhibitors or this norepinephrine can

undergo reuptake we have reuptake

Inhibitors such as tricyclic

antidepressants and cocaine remember

that Alpha 2 is anti-sympathetic we have

Alpha two agonists which decrease the

release of norepinephrine and we have

Alpha two antagonists which boost the

release of norepinephrine after

norepinephrine undergoes a reuptake it

can be degraded by Mao enzyme there is a

class of medications known as MAO

inhibitors guess what's going to happen

when I take an MAO inhibitor I will

decrease the degradation of

norepinephrine ending up with more

norepinephrine so we have direct acting

agonists which Target one or two

receptors we have mixed agonists which

Target many such as I am Alpha 1 and

Alpha 2 and Theta 1 and beta 2 agonists

such as Master epinephrine indirect

acting the releasers the enzyme

Inhibitors and the reuptake Inhibitors

some examples of alpha-1 agonists

include phenylephrine meteraminol

methane and midodrine and we shall not

forget methoxamine as for Alpha two

and others how about beta Agnes I have

isoproterinol beta 1 and beta 2 I have

albuterol which is beta 2 terabitaline

also beta 2. dobutamine for Motorola

cell motorol and metaproterinol just

like we have isoproterinol we have

metaproterinol too so this is how I

remember them isoproterinol with

metaproterenol okay we're good now what

dobutamine not to be confused with

dopamine we're good now what Albuterol

salbutamol turbitaline and then the

followed by mixed agonists epinephrine

is an Agonist on alpha-1 Alpha 2 beta 1

and beta 2 depending on the dose

norepinephrine is mainly alpha-1 Agonist

and some beta 1. some Alpha 2 exist as

well but not beta2 so epinephrine acts

on beta 2 but norepinephrine does not

how about dopamine look at the D it is

dy one Agonist it is beta1 Agonist and

Alpha One Agonist how about dobutamine

dobutamine does not touch the D at all

dobutamine is a beta 1 Agonist for the

most part phenoldopam is a D1 which is

dopamine receptor number one Agonist

let's start by talking about Alpha

agonists they include phenylephrine

methoxamine and others why do we use

them think about it if I am an alpha one

Agonist what's going to happen you will

vasoconstrict and when a vasoconstrict

what happens to the resistance the

resistance goes up and what happens is

the pressure the blood pressure goes up

so I can use them for hypotension

especially hypotension during spinal

anesthesia postural hypotension and

autonomic insufficiency what if I have

nasal congestion theoretically you can

take an alpha when Agonist 2

vasoconstrict the vessels and when

evasive constrict the vessels hopefully

I'll decrease the congestion because

congestion is caused by dilated vessels

that secrete mucus but can restricted

vessels usually secrete less mucus what

does the sympathetic nervous system do

to my pupils it dilates the pupils so if

I want to dilate the patient pupils I

can use one of these agents as for the

Alpha 2 agonists which are

anti-sympathetic we'll talk about them

in the next video which will be titled

sympatholytics beta agonists

isoproterenol works on beta 1 and beta

2. dobutamine is mainly an Agonist on

beta1 Albuterol salbutamol turbitaline

and the long-acting one salmon for

motorol or beta2 agonists if something

is beta two Agonist what do you think

it's going to do to my bronchi it will

dilate the bronchi and that's why they

can be helpful for asthma patients what

else well beta 2 will dilate or relax

the smooth muscles of the uterus so we

use them in precipitous labor or

premature labor hey baby stop stop don't

come out out yet so how do we relax the

uterus and stop the contractions to call

uses you give something like turbitaline

which is a beta2 Agonist next if

something is beta 1 Agonist oh beta 1 is

in the heart it will increase heart rate

and stroke volume so we can benefit from

them in some cases of heart failure if I

am a beta 1 Agonist I will raise the

heart rate so you can use me if you have

bradycardia and I can also increase

heart rate so you can use me if I have

hot block which is also bradycardia if

something is going to increase heart

rate and stroke volume what's going to

happen as a side effect tachycardia if

it has beta 2 what's going to happen to

my vessels remember that beta 2 are

inhibitory on everything they relax

everything they relax the vessels when I

like the vessels ivaseo dilate when I

evasio dilate the vessels in my face I

get flushing in my head I get headache

all over the body I get hypotension

because when I relax The Vessel what's

going to happen to to the radius the

radius goes up what's going to happen to

resistance resistance goes down and when

resistance goes down blood pressure goes

down as well beta 1 side effect

tachycardia even medications that are

mainly beta 2 can have some beta 1

activity so I get anxiety I get

palpitation next the big one nor

epinephrine nor epinephrine is a mixed

Agonist it acts as an Agonist an alpha

one alpha 2 and beta1 but mainly it's

Alpha One so if I stimulate Alpha 1

what's going to happen to my blood

vessels my blood vessels will constrict

so what's going to happen to the radius

radius decreases what's going to happen

to resistance resistance increases and

what's going to happen to the mean

systemic arterial blood pressure it

increases look here's the systolic

pressure before giving or epinephrine

here is the diastolic pressure before

giving norepinephrine the difference

between them is the pulse pressure as I

give norepinephrine and constrict the

vessels plus increasing the heart rate

and stroke volume a little the systolic

blood pressure goes is up the diastolic

blood pressure goes up and that means is

to make our chair blood pressure also

goes up how about the pulse pressure the

pulse pressure goes up as well why did

this systolic blood pressure go up like

this because it's Agonist on beta 1 and

Alpha One why did the dye start to go up

because nor Epi is Agonist on Alpha one

since nor Epi is Agonist on beta 1

what's gonna happen I can get increased

heart rate after the administration of

norepinephrine however why is the rise

in heart rate not huge because anytime

you raise your blood pressure you

stimulate your baroreceptors triggering

a vagal response and the vagus will try

to lower the heart rate and that's why

the heart rate does not increase a lot

and in some cases The Reflex bradycardia

can even win when you say that

norepinephrine is Agonist in all for one

is it constricting arteries or

constricting veins the answer is both it

is constricting almost every vessel in

your body except the coronary arteries

in fact norepinephrine and epinephrine

tend to dilate the coronaries I mean

think about it if you're exercising and

you have a wonderful healthy heart when

you run that's sympathetic world so

fight flight what happens epinephrine or

epinephrine get released from my Adrenal

medulla do you think your coronary

arteries will constrict or dilate well

since my heart needs more oxygen when I

exercise I better dilate the coronary

arteries proving that norepinephrine and

epinephrine do not construct the

coronaries okay nor epinephrine you will

constrict arterioles and veins let's

constrict arterials what's going to

happen to the afterload it increases

what happens to diastolic blood pressure

it increases what happens to the total

peripheral resistance it also increases

anytime you raise the blood pressure you

might trigger a better receptor reflex

and when you constrict veins what's

going to happen more venous return will

return to the right side of the heart so

what's going to happen to preload

preload goes up and diastolic volume

goes up and therefore there will be more

volume in the heart to pump more so

systolic blood pressure goes up anytime

you constrict veins what happens to

their compliance well since compliance

is similar to distensibility or

extensibility or capacitance the moment

I constrict my veins I decrease the

compliance I decrease expansibility I

decrease distensibility and I decrease

the capacitance of the veins what is

compliance again compliance is the

change in volume over the change in

pressure when I constrict my venules the

volume decreases when the volume

decreases the compliance decreases all

of this was the effect of noreprin alpha

1 which predominates at higher dose but

what's the effect of norepinephrine on

beta 1 it increases inotropy dromotropy

chronotropy it increases contractility

and therefore stroke volume volume and

therefore raises the systolic blood

pressure it increases the conduction

velocity and it increases heart rate

please note that we use norepinephrine

to treat hypotension because as you see

it raises the blood pressure we can use

norepinephrine after coronary artery

bypass graft because usually after

coronary artery bypass graft the vessels

dilate and the blood pressure drops to

prevent this we give norepinephrine to

raise the total peripheral resistance

what if I have septic shock while septic

shock has hypotension can we benefit

from norepi absolutely we need to

constrict those dilated vessels what's

the name of shock that happens in sepsis

is its hypovolemic shock is it called

eugenic Shock is it obstructive shock or

distributive shock please comment below

please note that nor epinephrine does

not act on beta 2 for the most part and

that's why it has very minimal Metabolic

Effect which may means it's not gonna

break down glycogen into glucose and

it's not gonna raise your blood sugar

when I give you anorepinephrine by

injection it's a very acidic medication

so we usually dilute it in a five

percent glucose solution which means if

I give you a hundred mL of solution with

the norepinephrine I will add 5

milligrams of glucose to it so that it's

5 over 100 or 5 percent some side

effects of norepi during infusion

extravasation can occur nor epinephrine

is a potent vasoconstrictor oh when I

evasive constrict the vessels there will

be less blood going to the cells which

means less oxygenated blood reaching the

cell and the cell will die from ischemia

I.E necrosis so how should I mitigate

this try not to inject nor epinephrine

locally but to inject it in a big veins

through a central venous line which is

connected to the right atrium because

the right atrium is your central vein

because it connects to that big biggest

veins in your body the superior vena

cava and inferior vena cava making the

right atrium the central vein that's why

we call the pressure in the right atrium

central venous brush what happens to

blood pressure when I give nor Epi blood

pressure goes up because I constricted

the arterioles and that's why it's

important to monitor the patient nor

epinephrine also constructs veins

increasing the venous return that's why

we should be very careful if I have

right ventricular failure because of the

right ventricle fails I.E cannot

contract and you overwhelm it with more

blood you will make the matter worse so

you gotta be cautious no epinephrine is

a constrictor on arteries and veins so I

increase the total peripheral resistance

or systemic vascular resistance and the

pulmonary vascular resistance and this

will increase the pulmonary artery

pressure nor epic acts on beta 1 raising

the heart rate and this so much

constriction can lead to what

hypoperfusion organ ischemia and organ

damage and and when the cell is toast

without oxygen it will shift to

anaerobic glycolysis anaerobic

glycolysis secretes lactic acid so I

developed lactic acidosis which causes

high anion gap metabolic acidosis how

should I mitigate this effect well well

well if nor epinephrine can lead to

ischemia and decrease blood supply to

the cell why don't you pump more volume

oh I don't get it remember that pressure

equals force over area that's true if

you give norepinephrine alone you

constrict vessels what happens the

surface area the surface area decreases

and the pressure increases because the

resistance went up however if I increase

the fluids or the force by giving you

more fluids with the norepinephrine you

will mitigate this effect and you will

end up with less resistance one of the

organs that is particularly vulnerable

to ischemia and in organ damage is the

kidney because there is a role that says

if there is no bpie perfusion to the

kidney there will be no ppie know your

information this is classic pre-renal

angiotemia which is a subtype of acute

renal failure the patient can suffer

from oligaria less urine formation or

anuria no urine the kidney without

robust perfusion is screwed forgive my

language we're done with norepinephrine

let's talk about epinephrine epinephrine

is only made by your Adrenal medulla not

by the nerve endings epinephrine action

Alpha 1 Alpha 2 beta 1 and beta2 it is a

mixed Agonist however this depends on

the dose at lower doses epinephrine acts

like isoproterinol mainly an Agonist on

beta 1 and beta 2 but at high dose of

epinephrine epinephrine acts like

norepinephrine meaning mainly on Alpha 1

and some Alpha 2 and beta 1. so

epinephrine low dose beta1 Agonist and

beta 2 Agonist if it's beta1 Agonist it

will increase all of the cardiac

properties like heart rate conduction

velocity and contractility raising the

stroke volume and the systolic blood

pressure anytime you raise the blood

pressure you will trigger a better

receptor reflex and get reflex

bradycardia epinephrine is an Agonist in

beta 2 dilating my bronchi improving my

asthma symptoms it also relaxes the

uterine muscle wall and it's not just

relaxing the muscles in the uterus and

the muscles in the bronchi but also the

smooth muscles in the blood vessel

decreasing the systemic vascular

resistance lowering the afterload

decreasing the diastolic blood pressure

and to a certain extent it might lower

the blood pressure but nor epinephrine

did not have any beta-2 function and

that's why norepinephrine can never

lower my blood pressure however

epinephrine can lower my blood pressure

next epinephrine acts on beta 2 which is

similar to Beta three so we can get

lipolysis or breakdown of lipids into

free fatty acids and glycerol we can

break down glycogen into glucose hashtag

glycogenolysis so it boosts

glycogenolysis and lipolysis how did it

boost glycogenolysis by stimulating the

enzyme phosphorylase glycogen

phosphorylase breaks down my glycogen

how do you break down the triglycerides

by activating triglyceride lipase and

other lipases at high dose however

epinephrine is similar to norepinephrine

it acts mainly on alpha-1 and then some

Alpha 2 and some beta 1. how can we

differentiate between epinephrine or

epinephrine remember that norepinephrine

did not have beta 2 agonism but

epinephrine is a beta 2 Agonist so the

way to uncover this is to block the

Alpha One let's block the alpha one so

epinephrine now cannot act on Alpha One

and neither can nor Epi okay who's gonna

Remain the betas Epi will act and beta 1

and beta 2 nor Epi will act only on beta

1 which means which one of these two is

more likely to dilate my vessels and

lower my blood pressure only epinephrine

but norepinephrine can not lower my

blood pressure recall that in the

beginning of this lecture we talked

about the fact that epinephrine is

similar to glucagon and cortisol and

thyroxine and all of these are

anti-insulin so it makes sense that if

you stimulate the sympathetic nervous

system you will inhibit insulin release

I mean look at this when I break down

glycogen do you think insulin approves

this no when I break down fat does

insulin like this no one last time

epinephrine at low dose is similar to

isoproterinol meaning it's beta1 Agonist

and beta 2 Agonist epinephrine at an

intermediate dose is an alpha-1 Agonist

and beta-2 Agonist at high dose it's

just like nor Epi mainly Alpha One and

some Alpha 2 and beta 1 and that's why

the effects on hemodynamics will be

slightly different put differently beta

predominates at lower dose but Alpha

predominates at higher doses what are

the clinical uses of epinephrine and

norepinephrine usually epinephrine is

used as an adjunct to local anesthetics

when I give the local anesthetics I want

them to remain local and not to spread

their bloodstream to other parts of the

body I want them to remain local okay if

you want them to remain local then

constrict The Vessel local if you can

shake the vessels locally the anesthetic

will not Escape it will remain here

locally that's why we give epinephrine

as an adjunct to local anesthetics to

prolong the effects of the local

anesthetic also if I have shock such as

septic shock blood pressure drops so

what should you do give me epinephrine

or epinephrine to raise my blood

pressure it does not have to be septic

shock it could be anaphylactic shock or

any other shock and in the patient with

shock we also give of intravenous fluids

what if I have a cardiac arrest or

cardiac block well epinephrine or

epinephrine can increase heart rate

contractility and conduction so we can

give epinephrine or epinephrine now the

following is only true for epinephrine

and not norepinephrine if I have

anaphylactic shock which usually means

shock and I cannot breathe because of

the bronchoconstriction epinephrine is

preferred because epinephrine has beta 2

which will dilate my bronchi but

norepinephrine does not dilate bronchi

next if I have asthma like status

asthmaticus should I benefit more from

Epi or nor Epi Epi why same thing I

dilate my bronchi with Epi not nor Epi

because Epi is Agonist on beta 2. there

you go epinephrine what do you do well I

can dilate your pupil because I am Alpha

One Agonist causing midoriasis and I am

Alpha One Agonist as well I can

constrict blood vessels hyperperfusion

the kidney is said no baby no peepee or

no perfusion no baby so I get oligaria

or anuria the hypo perfusion to the

kidney caused by epinephrine can be

stronger than that of norepinephrine

tachyphilaxis does not exist for

epinephrine what is tachyphylaxis it

means that the more doses I give you the

less the effect that I get oh so it is

kind of adaptation that's true it's

adaptation accolinization the more you

give the less you get but epinephrine

does not have that if I give epinephrine

again and again and again there is no

reduction in effect with repeated Doses

and that's why let's say that I'm

allergic to peanuts and I ate something

that had peanuts I developed

anaphylactic shock epinephrine can

rescue me today tomorrow next year next

decade Etc my body will never get used

to it this is not the case with other

synthetic non-catecholamines they have

some tachyphilaxis a referend broke down

the big sugar glycogen into glucose so

there is more glucose in the blood it

broke down the fat in the fat stores

into free fatty acids and glycerol in

the blood so the fat in the blood will

increase LDL increases in the blood

phospholipids increase lactate increase

insulin decreases because epinephrine

belongs to the glucagon world not the

insulin World epinephrine increases all

of the cardiac properties which increase

his myocardial oxygen consumption side

effects of epinephrine if you increase

myocardiac properties a lot and the

increase the myocardial oxygen

consumption a lot I can get acute heart

failure I can get pulmonary edema from

the acute heart failure I can get

arrhythmias from the tachycodia I can

get hypertension and the increase

myocardial oxygen consumption can make

me run out of oxygen leading to a

myocordial ischemia an important

pharmacology effect remember the normal

sodium potassium antibase what does it

do well it exists in in every cell it

pushes sodium out of the cell and pushes

potassium into the cell so normally

potassium is going in if I take a beta

Agonist I stimulate the sodium potassium

antibase so it works harder pushing more

sodium to the outside and more potassium

to the inside lots of potassium is

entering the cell less potassium is left

in the blood I get hypokalemia when I

take a beta Agonist conversely if I take

a beta blocker I block the sodium

potassium antipasa sodium will no longer

be able to live and potassium will be no

longer able to get in so all of that

potassium will remain outside causing

hyperkalemia so if I take Propranolol

metoprolol or any other olol I risk

developing hyperkalemia beta agonists

cause hypokalemia but beta blockers

cause hyperkalemia for the most part hey

dopamine what do you do I act on D1

receptor which dilates vessel remember

D1 dilates it dilates renal vessels

mesenteric vessels and coronary vessels

D1 receptors are GS coupled if you are

GS coupled you will stimulate ethylene

cyclase convert ATP to cyclic amp

activate protein kinase a which causes

vasodilation of smooth muscles

everything here is a adenylate cyclase

ATP cyclic amp protein kinase a dilate

the smooth muscles who else is GS

coupled remember beta1 GS beta 2 GS

couple beta 3 Gs coupled and D1 is also

GS coupled this was true for dopamine at

low dose dopamine at medium dose

increases all of the cardiac properties

because it starts to act on beta 1 which

is also GS coupled increases cyclic amp

next we have high dose of dopamine it

acts on D1 beta 1 and look at this Alpha

One appears raising my blood pressure

that's why we can give dopamine to

manage a patient in shock with

hypotension and we can give phenol dupem

to dilate vessels and lower my blood

pressure phenoldopam is a D1 Agonist

next ephedrine how do you work well

direct acting and indirect acting at the

end of the day I raise nor epinephrine

lots of norepinephrine will act on Alpha

receptors raising my blood pressure act

on beta receptor raise all of the

cardiac properties can the monoamine

oxidase enzyme present in my gut

metabolize ephedrine the answer is no so

can I give it orally yes I can have you

ever heard of oral epinephrine no how

about oral norepinephrine now how about

oral ephedrine yes it's not metabolized

by your gastric or intestinal now

ephedrine has slow inactivation and slow

excretion so it stays longer in your

body it has long duration can lead to

hyperglyce team yet not really can it

cause acidosis yes even more acidosis

than the drug that we'll discuss soon

which is phenylephrine which is also an

Agonist can it dilate my bronchi sure it

is beta Agonist can it act as a

decongestant let's try to figure out the

mechanism if it's also an Agonist it

will constrict blood vessels and if it

constricts blood vessels it decreases

congestion ephedrine is one of these

synthetic homies so it has tachyphilaxis

which means reduction in effect with

repeated doses phenylephrine another

synthetic homie synthetic

non-catecholamine less potent than nor

Epi phenylephrine is mainly an alpha-1

Agonist at lower dose at high dose

expect some Alpha to Agonist alpha-1

constricts vessels and raises my blood

pressure anytime blood pressure goes up

better receptor reflex gets triggered to

do the opposite to try to decrease blood

pressure by having reflex bradycardia so

hypertension and reflex bradycardia

sometimes during administration of

Anastasia or during surgery the

patient's blood pressure drops now can

we reverse this sure give phenylephrine

phenylephrine is Alpha when agonists it

will raise the blood pressure back to

normal phenylephrine might be helpful to

patients with coronary artery disease

because it improves coronary perfusion

just like EPI and nor Epi you can give

phenylephrine with nitric oxide to

improve oxygenation both of them improve

coronary perfusion and it depends on the

vessel because phenylephrine can

decrease blood flow to some vessels in

the kidney viscera and skin but increase

blood flow to vessels in the coronaries

and the pulmonary artery and this is one

of the reasons it improves oxygenation

what if I gave it too much phenylephrine

which is Alpha One Agonist how can I

resolve this give an alpha one blocker

or an alpha blocker such as phentolamine

in the next video we'll talk about

phentolamine and phenoxybenzamine quick

review on phosphodiesterase Inhibitors

also known as as inodators why Eno

because they increase conductivity y

dilators because they cause vasodilation

remember that if something is GQ coupled

such as alpha-1 receptors GQ equals

calcium equals contraction of smooth

muscles so bronchoconstriction

vasoconstriction constriction of

sphincters contraction of uterus Etc but

beta 1 beta 2 Beta 3 D1 and others are

GS coupled which means everything is a

adenylate cyclase convert ATP to cyclic

amp activate protein kinase a to the

what when it comes to cardiac muscles

I'm going to boost contractility when it

comes to smooth muscles I will relax

them I will dilate them vasodilation

bronchodilation uterus muscle relaxation

beta 1 on the kidney increases renin and

in the eye increases aqueous humor so we

talked about ATP ATP by adenylate

cyclase with the a will give me cyclic

amp also all right cyclic amp does what

bronchodilation vasodilation and

increase cardiac contractility and heart

rate oh then after cyclic amp performs

this function we degrade it into pieces

of trash or degradation products who

degraded cyclic amp

phosphodiesterase and we have many types

of phosphodized trays and many

medications that inhibit

phosphodiesterase so let's say that I

took Theophylline or malvernone or

amrenown or any of these phosphodization

Inhibitors I'll inhibit

phosphodiesterase raising the cyclic amp

which will relax my vessels relax my

bronchi increase heart rate and

contractility depending on the type and

the location of the phosphodious trace

so when I inhibit phosphodiesterase

cyclic amp goes up because it's not

degraded and it will cause

bronchodilation and vasodilation it will

increase heart rate and contractility

here is a phosphodite straight inhibitor

inhibit it's the degradation of cyclic

amp to cyclic amp increases so this is

similar to Beta agonists because beta

agonists also raise cyclic EMP a

phosphodized trace inhibitor raise a

cyclic amp what's the effect of cyclic

amp on different parts of the body well

when it comes to cardiac muscles I

increase cardiac contractility but when

it comes to smooth muscles I decrease

their contraction I dilate vessels I

dilate bronchi when cyclic amp increases

platelet aggregation decreases it's also

anti-inflammatory decreases your

triglycerides and increases your HDL the

so-called good cholesterol cyclic amp is

doozy think that you're running on a

treadmill your heart is increasing its

contractility but your vessels are

dilating to perfuse the Heart by

dilating the coronary and to perfuse the

skeletal muscles next quick review of

nitric oxide what does nitric oxide do

it activates guanine cyclase not

Adelaide cyclase everything here is G

instead of a go in a late cyclase GTP

gets converted to cyclic GMP activates

protein kinase G which activates

phosphatase which breaks down myosin

light chain phosphate into mice and

light chain I.E I remove the phosphate

when I remove the phosphate I will

inactivate the micellite chain I.E relax

it so nitric oxide relaxes the smooth

muscles in blood vessels including the

blood vessels of erectile tissue

hydralazine nitroproocide and nitrates

act similar to nitric oxide how about

sildenafilted anaphyl were danophil ooh

sayalis Viagra how do they work they

inhibit phosphodiesterase 5 decreasing

the degradation of cyclic GMP so I'll

have more cyclic GMP and more dilation

more relaxation of smooth muscles which

means more dilation and more erection

and that's why a will be a disaster to

take one of these medications with one

of these medications because if I take

them together I dilate too much and when

I dilate too much what's going to happen

to the radius radius goes up resistance

goes down blood pressure goes down and I

can die from severe hypotension never

ever combine a nitrate with acyl

thanophil can we take a moment to admire

all the medications that can erase

cyclic amp sure how about the

phosphodiesterase Inhibitors they can do

it so then I filter Dana filter and

Renown male Renown and I'm renowned

theophilins xanthine caffeine

silostazole dipyridamole all of them can

do it how about norepinephrine

epinephrine they are beta1 Agonist and

beta 1 is GS coupled which means it's

going to raise a cyclic MP isoproterenol

dopamine dobutamine all of these Ray

cyclic amp what's going to happen to my

heart increase all cardiac properties

heart rate and contractility heart rate

and stroke volume and what's going to

happen to the kidney able to create more

n which will raise my blood pressure and

what's going to happen to the smooth

muscles dilation relaxation

bronchodilation and vasodilation when I

take a phosphodiesterase inhibitor the

cyclic amp will go up cyclic amp goes up

meaning relaxation of smooth muscles oh

so the veins will relax and their

capacitance will increase so the blood

will pile up in my veins if blood is

piling up more in my veins it is not

reaching the right atrium it is not

reaching my central vein so what's going

to happen to the central venous pressure

it decreases the blood is piling up in

my veins it's not returning to the right

atrium so venous return decreases and

the pulmonary vascular resistance is

decreasing as well because I'm relaxing

the vessels when you relax the vessels

the radius goes up but the resistance

goes down just like that what else do

phosphodized Trace Inhibitors do they

boost cardiac contractility leaving less

fluid or less blood accumulating in The ventricle so the left ventricular end

ventricle so the left ventricular end diastolic pressure decreases less blood

diastolic pressure decreases less blood accumulating in the left ventricle means

accumulating in the left ventricle means less blood accumulating in my left

less blood accumulating in my left atrium so the left atrial pressure I.E

atrium so the left atrial pressure I.E the pulmonary capillary which pressure

the pulmonary capillary which pressure decreases how do they do this by

decreases how do they do this by boosting cardiac conductivity so cardiac

boosting cardiac conductivity so cardiac contractility increases stroke volume

contractility increases stroke volume increases cardiac output increases heart

increases cardiac output increases heart rate increases what does cyclic amp do

rate increases what does cyclic amp do to blood vessels it relaxes blood

to blood vessels it relaxes blood vessels when you relax blood vessels the

vessels when you relax blood vessels the resistance decreases and the blood

resistance decreases and the blood pressure can decrease as well look at

pressure can decrease as well look at this m renowned Mildred known in

this m renowned Mildred known in ambrenone how do they work they inhibit

ambrenone how do they work they inhibit phosphodiesterase 3 which means cyclic

phosphodiesterase 3 which means cyclic amp will not be broken down increased

amp will not be broken down increased cyclic amp will lead to activation of

cyclic amp will lead to activation of protein kinase a because everything here

protein kinase a because everything here is a I will open the calcium channels in

is a I will open the calcium channels in the cardiac myocyte which means more

the cardiac myocyte which means more calcium will rush into the cardiac

calcium will rush into the cardiac muscles calcium induced calcium release

muscles calcium induced calcium release calcium is the hero of a contraction so

calcium is the hero of a contraction so I get increased contractility and that's

I get increased contractility and that's how amberenone melanone and inambra

how amberenone melanone and inambra known can boost cardiac contractility

known can boost cardiac contractility and increase the stroke volume which

and increase the stroke volume which increases the cardiac output which may

increases the cardiac output which may increase my blood pressure so M Renown

increase my blood pressure so M Renown in Amber known mirror known make my

in Amber known mirror known make my ventricle contract stronger when I

ventricle contract stronger when I contract stronger I get rid of all of

contract stronger I get rid of all of that blood I eject that blood quickly so

that blood I eject that blood quickly so less blood will accumulate in my right

less blood will accumulate in my right atrium and my right atrial pressure will

atrium and my right atrial pressure will decrease okay so less pressure here less

decrease okay so less pressure here less pressure in the right ventricle less

pressure in the right ventricle less pressure in the pulmonary artery so my

pressure in the pulmonary artery so my pulmonary artery pressure will also

pulmonary artery pressure will also decrease however M renowned in amrenome

decrease however M renowned in amrenome Middle Renown are increasing

Middle Renown are increasing contractility what happens to cardiac

contractility what happens to cardiac output increases what happens to the

output increases what happens to the cardiac index which is a type of cardiac

cardiac index which is a type of cardiac output it increases how about the left

output it increases how about the left ventricle stroke index it increases left

ventricle stroke index it increases left ventricular ejection fraction it

ventricular ejection fraction it increases when you pump blood stronger

increases when you pump blood stronger you will have less blood accumulating in

you will have less blood accumulating in the left ventricle so what's going to

the left ventricle so what's going to happen to left ventricular and diastolic

happen to left ventricular and diastolic pressure it decreases less blood

pressure it decreases less blood accumulating in the left ventricle means

accumulating in the left ventricle means less blood will pile up in the left

less blood will pile up in the left atrium so what's going to happen to the

atrium so what's going to happen to the left atrial pressure or the pulmonary

left atrial pressure or the pulmonary capillary wedge pressure it decreases

capillary wedge pressure it decreases and what's going to happen to the

and what's going to happen to the systemic vascular resistance usually

systemic vascular resistance usually decreases because remember when I

decreases because remember when I increase cyclic amp I dilate the vessels

increase cyclic amp I dilate the vessels so hypotension is more common than

so hypotension is more common than hypertension so now I want you to pause

hypertension so now I want you to pause and review here are the answers remember

and review here are the answers remember that the half-life of ambranone is about

that the half-life of ambranone is about three hours there is no tachyphilaxis

three hours there is no tachyphilaxis here just like epinephrine it gets

here just like epinephrine it gets metabolized in the liver by an

metabolized in the liver by an acetylation and glucose iranidation

acetylation and glucose iranidation remember in the last video when we

remember in the last video when we talked about anti-seizure medications we

talked about anti-seizure medications we talked about for macokinetics absorption

talked about for macokinetics absorption distribution metabolism excretion the

distribution metabolism excretion the metabolism of ambranone occurs in the

metabolism of ambranone occurs in the liver M renowned in Amity known do two

liver M renowned in Amity known do two things they boast cardiac contractility

things they boast cardiac contractility and they lower blood pressure so they

and they lower blood pressure so they are beneficial in cardiac surgery

are beneficial in cardiac surgery coronary artery bypass graft because in

coronary artery bypass graft because in many of these cases there is vasospasm

many of these cases there is vasospasm oh oh I do not want vasopasm I want to

oh oh I do not want vasopasm I want to dilate the vessels and lower the

dilate the vessels and lower the resistance that's when M Renown or

resistance that's when M Renown or enambranone might be beneficial side

enambranone might be beneficial side effects if you dilate too much you drop

effects if you dilate too much you drop the blood pressure they can decrease

the blood pressure they can decrease plated aggregation because they boost

plated aggregation because they boost cyclic amp and they can lead to cardiac

cyclic amp and they can lead to cardiac arrhythmias because they increase the

arrhythmias because they increase the stroke volume too much and let's put

stroke volume too much and let's put everything together here in this table

everything together here in this table these are the sympathomimetics in the

these are the sympathomimetics in the next video in this pharmacology playlist

next video in this pharmacology playlist we shall talk about sympatholytics

we shall talk about sympatholytics please take a moment to pause and review

please take a moment to pause and review the name of each medication and the

the name of each medication and the mechanism of actions very important

mechanism of actions very important quick review of the medications

quick review of the medications methylpetyrosine prevents the synthesis

methylpetyrosine prevents the synthesis of neurotransmitters rather pain

of neurotransmitters rather pain prevents the entry of the norepinephrine

prevents the entry of the norepinephrine into the vesicle bertilium and

into the vesicle bertilium and guanathidine prevents the release of the

guanathidine prevents the release of the neurotransmitter amphetamine and

neurotransmitter amphetamine and terabenes are the opposite they boost

terabenes are the opposite they boost the release of the norepinephrine

the release of the norepinephrine tricyclic antidepressants and cocaine

tricyclic antidepressants and cocaine prevent the reuptake of norepinephrine

prevent the reuptake of norepinephrine they are reuptake Inhibitors MAO

they are reuptake Inhibitors MAO inhibitors prevent the metabolism of

inhibitors prevent the metabolism of norepinephrine

norepinephrine comt Inhibitors are similar the alpha

comt Inhibitors are similar the alpha Agonist beta agonis Etc they act on The

Agonist beta agonis Etc they act on The postsynaptic receptors in the next video

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YouTube Transcript:Sympathomimetics (Adrenergic Agonists)—Epinephrine, Norepinephrine - Alpha & Beta Receptors

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Sympathomimetics (Adrenergic Agonists)—Epinephrine, Norepinephrine - Alpha & Beta Receptors