The renin-angiotensin-aldosterone system

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The Renin-angiotensin-aldosterone system (RAAS, renin-angiotensin-aldosterone axis) is one of the main neurohumoral regulators of physiological homeostasis. The primary stimulus for its activation is the outflow of renin from juxtaglomerular cells, located in the media of afferent renal arterioles. This can happen based on:

  • decreased blood flow through afferent arteriole (eg hypotension of various etiologies, renal artery stenosis);
  • reduction of NaCl supply to the macula densa region of the distal tubule;
  • activation of β1-adrenoreceptors in the region of juxtaglomerular cells.
    The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS)

Renin secretion is also stimulated' by prostaglandins (PGI2, PGE2). On the other hand, renin secretion is inhibited by β-blockers.

Mechanisms of transformations[edit | edit source]

The main function of renin is the cleavage of the decapeptide angiotensin I (AGI) from angiotensinogen. Histidine and leucine in positions 9 and 10 are subsequently cleaved from angiotensin I by angiotensin-converting enzyme (ACE). This results in the octapeptide angiotensin II (AGII). Conversion diagram and function of AGII see picture.

  1. AGII causes significant vasoconstriction predominantly in the arteriolar blood stream, with a lesser intensity it also affects the veins. Vasoconstriction is most evident in the skin and kidneys. At least, on the contrary, it affects the vessels of the brain and muscles.
  2. In the kidneys, AGII leads to vas efferens constriction and by a not entirely clear mechanism, it increases sodium reabsorption in the proximal tubule.
  3. In the adrenal cortex, it stimulates the release of aldosterone, which subsequently potentiates the reabsorption of sodium and the excretion of potassium in the distal tubule and collecting duct.
  4. In the adrenal medulla, AGII facilitates the release of catecholamines.
  5. Centrally increases sympathetic tone (stimulates the release of catecholamines from nerve endings).
  6. In the neurohypophysis, AGII stimulates the secretion of vasopressin' (ADH) with subsequent water retention. Most of these effects are mediated by the binding of AGII to the specific AT1-receptor.
  7. With a long-term increase in the concentration of AGII, its strong pro-oncogenic effect' is manifested - the growth of vascular smooth muscle cells and striated heart muscle is stimulated, the synthesis of collagen increases and the production increases superoxide radicals.


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