Renin-angiotensin-aldosterone system

In addition to the mechanisms of the osmotic sensor and effector, water-salt metabolism in the human body is regulated by the mechanisms of the volumetric sensor and effector, the main of which is the renin-angiotensin-aldosterone system.

Renin, synthesized by the juxtaglomerular apparatus of the kidney, is a proteolytic enzyme that catalyzes the breakdown of angiotensinogen, synthesized in hepatocytes into decapeptide – angiotensin I. Angiotensin I does not have vasoconstrictive or mineralocorticoid activity, but doesn’t apply to the lung angiotensin; significant vasopressor activity. The product of angiotensin II metabolism is angiotensin III. Angiotensin II and angiotensin III act via cell surface receptors on the cells of the glomerular zone of the adrenal glands, activate protein kinase C, with subsequent activation of the synthesis of pregnenolone and aldosterone (Aguilera e.a, 1980; Catt e.a, 1979; Kramer e.a, 1980 ). Aldosterone acts on target tissue,expressing nuclear mineralocorticoid receptor to stimulate sodium absorption and potassium excretion. To control the volume of intravascular fluid, the primary target of aldosterone action is the distal non-front. Here, aldosterone increases the synthesis of the sodium channels of the apical membrane, mitochondrial enzymes involved in the synthesis of ATP, and the Na +, K + components of ATP-ase to increase sodium reabsorption and the excretion of potassium.

Natriuretic peptide system

In addition to the classical systems involving vasopressin and the renin-angiotensin-aldosterone system, the salt-water balance is regulated by the natriuretic peptide system. The effects of this system are manifested both at the level of the central nervous system by influencing the secretion of vasopressin, as well as at the periphery, by directly stimulating the excretion of sodium in the kidneys and indirectly suppressing the production of aldosterone by the adrenal glands.

local_offerevent_note November 6, 2019

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