ACE inhibitors also lead to the increased production of bradykinin – which is a vasodilator. Excessive angiotensin II can also lead to large inflammatory changes such as cytokine-induced organ damage in addition to increased membrane permeability and epithelial cell apoptosis.Īs angiotensin II is a vasoconstrictor, alleviation causes vasodilation thus reducing systemic blood pressure levels. ACE inhibition prevents the conversion of angiotensin I to angiotensin II, thus keeping angiotensin inactive.Īngiotensin II binding to AT 1R can also induce cardiac dysfunction including hypertrophy, arrhythmia, and ventricle function failure. Abnormally active RAAS leads to chronic hypertension and thus the high blood pressure needs to be counterbalanced.ĪCE inhibitors are commonly used drugs in the treatment and management of hypertension and heart failure. Primary pathologies of impaired RAAS include chronic hypertension, kidney, and cardiac failure. The retention of water and sodium leads to increased blood volume, and thus blood pressure. Image Credit: StudioMolekuul/ AldosteroneĪngiotensin II stimulates the secretion of aldosterone is produced by the zona glomerulosa of the adrenal cortex (adrenal gland) and is involved in the retention of sodium in the kidney and other glands. By acting on the pituitary gland, angiotensin II also stimulates the secretion of vasopressin also known as antidiuretic hormone, which increases water retention in the kidneys by adding water channels (aquaporin) to the collecting duct.Īngiotensin II structure. Furthermore, these events can also lead to insulin resistance and thrombosis, whereas binding to AT 2R has opposing effects: vasodilation reduced platelet aggregation and enhanced insulin activity.Īngiotensin II also acts on the brain where it can bind to the hypothalamus to stimulate thirst to increase water intake. Normally, if blood pressure is too high, atrial natriuretic peptide (ANP) – secreted by cardiac muscle cells – leads to reductions in blood volume, leading to reduced blood pressure.Īngiotensin II binding to AT 1R can result in a cascade of inflammation, constriction, and the promotion of atherosclerosis. Angiotensin II is a potent vasoconstrictor, which leads to increased blood pressure. ACE is primarily found in vascular endothelia of the lungs and the kidneys.Īngiotensin II binds to angiotensin type I A (AT 1AR) or B (AT 1BR), as well as type II (AT 2R) receptors. Angiotensin-converting-enzyme (ACE) further cleaves angiotensin I to form angiotensin II – which is the primary active peptide of RAAS. Renin acts on angiotensin (continuously produced by the liver) to cleave a 10 amino acid peptide from the N-terminus to form angiotensin I (inactive). Decreased blood pressure activates juxtaglomerular cells, which leads to prorenin being cleaved into its active form – renin, which is then secreted into the bloodstream. Juxtaglomerular cells in the kidney are abundant in an inactive precursor protein called prorenin which is constantly secreted. Typically, RAAS is activated when there is a drop in blood pressure (reduced blood volume) to increase water and electrolyte reabsorption in the kidney which compensates for the drop in blood volume, thus increasing blood pressure.
RAAS regulates sodium and water absorption in the kidney thus directly having an impact on systemic blood pressure. The RAAS is a complex multi-organ endocrine (hormone) system involved in the regulation of blood pressure by balancing fluid and electrolyte levels, as well as regulating vascular resistance & tone. Image Credit: kurhan/ What is the renin-angiotensin-aldosterone system (RAAS)? Dysregulated RAAS is implicated in high blood pressure, cardiovascular and kidney conditions, and medications targeting RAAS can improve these conditions.ĭysfunction of the RAAS is also thought to be implicated in COVID-19 severity and targeting RAAS may be a potential therapeutic strategy for COVID-19 complications. The renin-angiotensin-aldosterone system (RAAS), or renin-angiotensin-system (RAS) is a regulator of blood pressure and cardiovascular function. Osman Shabir, PhD Reviewed by Sophia Coveney
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