0:09 All right, ninjaers. So, we talked in
0:11 great detail about the adrenal gland,
0:14 right? We went over in a lot a lot of
0:16 specific details. What I want to do now
0:18 is I just want to get a quick overview
0:20 of the adrenal gland. What stimulates
0:22 it? What's its target organs and some of
0:25 the negative feedback mechanisms? Okay.
0:26 All right. So, where do we have to
0:27 start? We have to start in the
0:28 hypothalamus. Now there's a specific
0:31 nucleus located in the hypothalamus and
0:34 again uh it's the the nucleus that's
0:36 actually going to be in this area. If I
0:37 were to draw here's the actual neuron
0:41 here. It secretes what hormone? This
0:44 hormone that it secretes is called
0:46 corticotropen releasing hormone. What's
0:48 the nucleus that actually secretes? This
0:51 is the par ventricular nucleus. What
0:53 does the corticotropen releasing hormone
0:54 do? It circulates down through the
0:57 hypoicial portal system and stimulates
1:02 specific cells located in the anterior
1:04 pituitary. Those are called
1:05 corticotropes. And when the
1:07 corticotropin releasing hormone
1:08 circulates down through the
1:11 hypoasoportal system and stimulates this
1:13 corticotrope, the corticotrope secretes
1:15 two different chemicals. One we're going
1:17 to focus on and one we're not going to
1:19 talk about. One is alpha MSH because we
1:21 talked about that in the large detailed
1:24 video. And then the important one which is
1:25 is
1:27 adreninocorticotropic hormone. All
1:28 right. So now what's the function of
1:31 adreninocorticotropic hormone. Okay.
1:32 Adreninocorticotropic hormone can go to
1:35 this adrenal gland here. Right? So the
1:37 adrenal gland has two components that we
1:38 talked about. If you look at these blue
1:40 cells, these red cells and these green
1:42 cells. All of these three layers make up
1:46 what's called the adrenal cortex. And in
1:48 the middle of the adrenal gland is going
1:50 to be the adrenal medulla. So what does
1:52 adrenalcorticotropic hormone do? Let's
1:55 follow it to the adrenal cortex. So it
1:57 comes over here, circulates through the
1:59 blood and it acts on a bunch of
2:01 different receptors on these cells,
2:03 right? So let's go ahead and remember
2:05 these basic cells here. What was this
2:07 blue cell layer here called? This blue
2:10 cell layer here was called the zona
2:13 glomemeilosa. This red cell layer here
2:16 is called the zona
2:18 faciculada. And this green cell layer
2:20 here is going to be the zona
2:22 zona
2:24 reticularis. What the
2:26 adreninocorticotropic hormone does is is
2:29 it can act on all of these three cells.
2:31 So let's show that here. Look, it's
2:33 coming in here and it bifurcates and it
2:37 can act on these three cells. So it can
2:40 stimulate the zona reticularis. It can
2:42 stimulate the zonop facicula and it can
2:45 stimulate the zona glmeilosa. Now there
2:47 is other stimuli here. We'll talk about
2:49 that in just a second. What is the zonog
2:51 glomemeillosa responsible for
2:54 secretreting? It secretes chemicals and
2:56 these chemicals are controlling your
2:59 mineral balance. So they're called
3:03 mineral corticoids, right? What was the
3:05 main one that we talked about?
3:07 Aldoststerone, right? And we'll talk
3:09 about him in just a second and his
3:12 effects. Then what else? Acetal I'm
3:14 sorry adrenalcorticotropic hormone can
3:17 act on the zonop faciciculata and it can
3:19 stimulate the zonopiculata to control
3:22 certain types of metabolic activities
3:24 with respect to glucose right and these
3:29 gluccocorticoids. Now the specific one
3:32 that we talked about is
3:35 cortisol. Okay. And then it can also the
3:37 adrenal corticotropic hormone can
3:40 stimulate the zona reticularis to
3:41 produce things that are risk going to
3:43 affect your gonads of the ovaries and
3:47 the testes and these are called
3:50 gonadoc corticoids. Now we talked about
3:51 these already. We're just going to call
3:54 them androgens, right? But the specific
3:59 ones were androone dione and DHEA
4:01 dehydroepiendostrone. Okay, now that
4:03 we've done that, what is some other
4:05 stimuli here for the zona glomemeillosa?
4:07 Because I want to talk about him too.
4:09 It's not just the adrenal corticotropic
4:10 hormone because he was one of the big
4:12 ones, right? So again, what hormone is
4:14 stimulating this process here? We were
4:16 to follow it out here. It's the adrenal
4:19 corticoot tropic hormone, right? What is
4:22 it doing? It's acting on these zonos,
4:24 zona facicula and zon reticularis.
4:26 There's other signals here. What is
4:29 these other signals here? Other things
4:31 could be for the zona glomemeilosa could
4:35 be angio tensin 2. What is another
4:39 signal here? It could be low plasma
4:42 sodium ions and high potassium ions in
4:45 the plasma. Right? And this is
4:47 stimulatory. This is stimulatory. But
4:49 they can also receive another signal
4:51 here. It's not significant. It's from
4:53 atrial nectaratic peptide and it's
4:57 inhibitory. Now angotensin 2, we talked
4:59 about him already. He's important for
5:00 being able to increase your blood
5:02 pressure. These sodium ions are helping
5:04 to stimulate the production of
5:06 aldoststerone and atriatriotic peptide
5:07 is trying to inhibit the production of
5:10 eldoststerone and adreninocorticotropic
5:12 hormone can have an effect on the
5:15 zonoglossa to produce aldoststerone. All
5:16 right. So, we've made all of these
5:19 different types of sex hormones, uh,
5:22 gluccocorticoids and mineral corticoids.
5:24 One more thing is the adrenal medulla.
5:25 So, if you look here in the adrenal
5:28 medulla, we already talked about him.
5:30 He's actually made up of nervous tissue,
5:33 right? So, neural tissue. So, he has the
5:35 post gangleionic motor neurons in here.
5:36 And when it's stimulated stimulated by
5:38 the sympathetic nervous system, right,
5:40 through the thoracco lumbar output, it
5:43 can secrete what? What are the chemicals
5:47 it secretes? Epinephrine and
5:48 norepinephrine. And we talked about
5:50 these in great detail, right? They help
5:52 to be able to stimulate
5:54 gluconneogenesis, glycogenolyis, and
5:56 lipolysis, right? And increase your
5:58 blood pressure. Okay? So, what are these
6:02 guys' effects in whole? increase BP increase
6:03 increase uh
6:05 uh glyco
6:13 genois and they increase what's called gluco
6:19 neoenesis and they increase what's called
6:21 called
6:24 lipolysis. Okay, now we've done these
6:27 guys. What's the effect of mineral
6:29 corticoids? Let's look at it over here.
6:31 So what was that hormone that we talked about?
6:32 about?
6:35 Aldoststerone. He affects the kidney
6:36 specifically in the distal convoluted
6:38 tubule, right? And what's his overall
6:42 function? He helps to be able to create
6:45 sodium reabsorption. So pull sodium from
6:46 the kidney tubules into the blood,
6:49 right? And then he excretes out
6:51 potassium. But as a result of the sodium
6:55 moving in, who else follows? Water. So
6:57 what's the overall result here? you
7:00 increase blood volume and you increase
7:03 blood pressure. Okay? And you also
7:06 increase the sodium content. All right?
7:08 So you end up what's called hyper
7:11 hyper
7:13 nitreia. Okay? But this could you know
7:14 not necessarily
7:16 pathological. Okay. What was the other
7:18 thing over here? It was with respect to
7:22 cortisol. So here's our cortisol over
7:24 here. Right? So cortisol did a lot of
7:27 things. What did it do? It act on the
7:29 white blood cells, your immune system.
7:30 What does it do to the immune system? It
7:33 suppresses the immune system, right? By
7:34 inhibiting the release of a lot of different
7:35 different
7:38 cytoines. So, it suppresses the immune
7:41 system. What does it do to the muscles?
7:43 You remember it's actually a very very
7:45 chronic stress hormone, right? So, it
7:48 can assist in what's called protein
7:50 protein
7:52 catabolism. So, it can break down
7:54 proteins into amino acids. What can it
7:57 do here to the fat tissue? It can cause
7:58 the fat tissue to
8:01 undergo lipolysis, right? So, it breaks
8:04 down triglycerides into fatty acids and
8:07 glycerol. And it can stimulate the liver
8:09 to do what's called a very very
8:12 important process and that process is called
8:14 called gluco
8:21 neoenesis. Okay? Okay, so it can take
8:23 amino acids and convert amino acids into
8:25 glucose. It can take glycerol and
8:26 convert it into glucose. Tons of
8:29 different things here, right? And it can
8:31 also enhance the sympathetic nervous
8:33 systems effects, right? By increasing
8:35 the adinuric receptors. All right, so
8:38 that's cortisol. All right, so we talked about
8:39 about
8:42 cortisol, we talked about asterostrone,
8:43 we talked about epinephrine and nor
8:45 epinephrine. Let's finish up with these
8:47 gonatorticoids. They're nothing that
8:48 we're going to spend a lot of time on.
8:50 And the reason why is they're so
8:52 insignificant. They're very very weak. I
8:55 should actually put here very
8:59 weak. But what they do is they can these
9:02 androgens can act as precursors. So if
9:03 for example, if I wanted to go to the
9:06 female, it could be used to make
9:09 estrogen. If I take it to the male, the
9:12 male can use that to make it into testosterone.
9:13 testosterone.
9:16 But their overall functions of the
9:18 gonatocorticoids primarily if we were to
9:20 just kind of overly their entire
9:23 function is to control libido. So sex
9:26 drive. Okay. All right. So now now that
9:28 we know that we understand what cortisol
9:29 does, eldoststerone does and
9:32 gonadocorticoid does. Now real quickly
9:34 here with the cortisol, this is the one
9:36 I really want to talk about. If you're
9:37 making because what happens
9:39 adreninocorticotropic hormone stimulates
9:42 your zonopiculata to make cortisol. What
9:44 happens if your cortisol levels rise
9:47 really really high? They exert a
9:49 negative feedback mechanism. So let's
9:52 say here's our cortisol. It exhibits a
9:54 negative feedback mechanism. What do you
9:56 do? You make less corticotropen
9:58 releasing hormone. You make less
10:00 adreninocorticotropic hormone and then
10:02 that triggers the the zonopiculata to
10:06 not make as much cortisol. That's that
10:07 negative feedback mechanism. Now, if it
10:09 was the exact opposite, if there's less
10:11 cortisol, there's going to be less
10:13 inhibitory input, right? So, there's
10:14 going to be less of that negative
10:16 feedback mechanism there. It's going to
10:18 cause them to make what? More
10:20 corticotropen releasing hormone. More
10:22 corticotropin releasing hormone will
10:23 actually stimulate the antipituitary
10:27 gland to make more act. And more ACT
10:28 will stimulate the zonal physiculata to
10:31 make more cortisol. All right guys, so I
10:32 hope that made sense. In this video, we
10:34 covered a general overview of all the
