RAAS (renin-angiotensin-aldosterone system)

How is RAAS structured and how does it work?

The system includes the following key components:

• Renin is a proteolytic enzyme (protease). It is secreted by the juxtaglomerular cells of the kidneys. It cleaves a peptide from angiotensinogen to form angiotensin I.
• Angiotensin II is a potent vasoconstrictor that exerts a pronounced blood vessel-narrowing effect. It is a dipsogenic substance: it stimulates water intake, i.e., thirst. It interacts with membrane receptors on target cells (AT1 and AT2), increases sympathetic nervous system tone, and stimulates aldosterone secretion.
• Aldosterone is a mineralocorticoid of the adrenal cortex. It stimulates the reabsorption of sodium ions ($Na^+$) and the secretion of potassium ions ($K^+$) in the renal tubules.

How does the system regulate blood volume and pressure?

RAAS is involved in the regulation of blood pressure and water-salt metabolism.

The compensation mechanism during hypovolemia and blood pressure drop includes the following links:

1. A decrease in circulating blood volume triggers the activation of ADH; narrowing of interlobular arteries and afferent arterioles decreases glomerular filtration and leads to ischemia of the juxtaglomerular apparatus cells.
2. Ischemia of the JGA induces the secretion of renin, which leads to the formation of angiotensin II.
3. Angiotensin II increases arteriolar tone, stimulates the release of catecholamines, and activates the secretion of aldosterone.
4. Aldosterone stimulates $Na^+$ reabsorption in the tubules.
5. An increase in blood $Na^+$ causes plasma hyperosmolarity, excitation of vascular osmoreceptors, and additional stimulation of ADH secretion by the hypothalamus.
6. Result: fluid flow into the blood vessels increases and plasma volume is restored.

How do RAAS parameters change during pregnancy?

During pregnancy, RAAS parameters change:

• The level of angiotensin II increases 2–3 fold.
• Plasma renin activity increases 2–4 fold.
• Plasma and urine aldosterone content increases 3-fold in the 1st trimester and up to 10-fold by the 3rd trimester.

What is the role of RAAS in the development of pathologies?

RAAS is involved in a number of pathological conditions:

• Blood loss: during hydremic compensation of blood loss, JGA ischemia causes renin secretion and angiotensin II formation; aldosterone stimulates $Na^+$ reabsorption, which helps restore plasma volume.
• Arterial hypertension: RAAS belongs to pressor mechanisms. Renin → angiotensin II → aldosterone; the system leads to $Na^+$ retention and an increase in circulating blood volume.
• Urinary pathology: RAAS activation during the suppression of the prostaglandin and kallikrein-kinin systems is associated with sodium and water retention, hypervolemia, hypernatremia, and an increase in total peripheral vascular resistance.
• Chronic heart failure: decreased left ventricular systolic function is accompanied by the activation of pressor systems, including the RAAS. Hemodynamic effects of neurohumoral factors: peripheral vasoconstriction and sodium and fluid retention, which increases pre- and afterload on the left ventricle. Stimulation of fibrosis and cardiomyocyte apoptosis is also described.
• Pharmacological effects: medicinal lowering of blood pressure triggers compensatory mechanisms of sodium and water retention. Lowering blood pressure reduces renal blood flow, increases renin secretion, activates angiotensin II formation, increases aldosterone secretion, and leads to sodium and water retention.

Class and exam questions

What else to study on this topic

• Sympathoadrenal system (SAS)
• Antidiuretic hormone (vasopressin)
• Juxtaglomerular apparatus of the kidney
• Blood pressure regulation

Other topics in "Physiology concepts"

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