The renin–angiotensin–aldosterone system, RAAS, is a hormonal system that controls blood
pressure.
While baroreflex is a short-term response to sudden changes in blood pressure, RAAS
is responsible for long-term regulation.
In the kidneys, within the walls of afferent arterioles, there are specialized cells producing
prorenin called juxtaglomerular cells.
Upon activation by a drop in blood pressure, prorenin is cleaved to form renin, which is
released into the blood.
Renin converts a plasma protein called angiotensinogen, produced by the liver, into angiotensin I,
a peptide of 10 amino acids.
Angiotensin I is further converted into angiotensin II, an 8-amino acid peptide, by the angiotensin-converting
enzyme, ACE, predominantly present in the lungs and kidneys.
Angiotensin II is a hormone.
It binds to angiotensin II receptors in tissues to exert various effects:
- It promotes sodium reabsorption in proximal convoluted tubules of the kidneys.
- It stimulates vasoconstriction in systemic arterioles.
- It induces the release of aldosterone from the adrenal cortex.
Aldosterone promotes sodium and water retention in the kidneys.
- In the central nervous system, angiotensin II has several effects:
+ It acts on the hypothalamus to stimulate thirst and encourage water intake.
+ It induces the posterior pituitary to release antidiuretic hormone, which promotes water
retention by the kidneys.
+ It reduces the sensitivity of the baroreceptor response to increased blood pressure, so that
this response would not counteract the effect of RAAS.
All these actions lead to an increase in blood volume and blood pressure.
Angiotensin II is short-lived with a half-life of 1 to 2 minutes.
It is degraded into angiotensin III and IV, which have lesser effects.
Overactive or inappropriately activated RAAS is a cause for hypertension.
RAAS is a frequent target of anti-hypertensive drugs.
ACE inhibitors and angiotensin receptor blockers are common treatment for hypertension.
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