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Angiotensin II is the major bioactive product of the renin–angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them; and to receptors on the zona glomerulosa cells, causing the release of aldosterone from the zona glomerulosa in the adrenal cortex.
Vitamin D inhibits renin secretion and its activity, it therefore acts as a "negative endocrine regulator of the renin–angiotensin system". Hence, a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma. [32]
Renin (Primarily) Juxtaglomerular cells: Activates the renin–angiotensin system by producing angiotensin I of angiotensinogen: Erythropoietin (EPO) Extraglomerular mesangial cells: Stimulate erythrocyte production Calcitriol (1,25-dihydroxyvitamin D 3) Proximal tubule cells Active form of vitamin D 3
Vitamin D is a group of structurally related, fat-soluble compounds responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, along with numerous other biological functions. [1] [2] In humans, the most important compounds within this group are vitamin D 3 (cholecalciferol) and vitamin D 2 (ergocalciferol). [2] [3]
Anatomical diagram of the renin–angiotensin system, showing the role of ACE at the lungs [11] ACE is also part of the kinin–kallikrein system where it degrades bradykinin, a potent vasodilator, and other vasoactive peptides. [12] Kininase II is the same as angiotensin-converting enzyme. Thus, the same enzyme (ACE) that generates a ...
Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in the kidneys' salt and water handling (particularly abnormalities in the intrarenal renin–angiotensin system) [82] or abnormalities of the sympathetic nervous system. [83]