The half-life of angiotensin II in circulation is very short, less than 60 seconds. Angiotensin II is the primary mediator of the physiologic effects of RAAS, including blood pressure, volume regulation, and aldosterone secretion. It cleaves the two amino acids from the C-terminal of angiotensin I to make the peptide angiotensin II.ĪCE generates angiotensin II by cleaving the two amino acids at the C-terminal of angiotensin I. This enzyme is expressed on plasma membranes of vascular endothelial cells, primarily in the pulmonary circulation. This peptide does not have any known biological activity. Renin cleaves the N-terminal of angiotensinogen and leads to the formation of angiotensin I. This molecule is primarily synthesized and constitutively secreted by the liver. Renin is the rate-limiting enzyme in RAAS. The half-life of renin activity in circulation is 10-15 minutes. Therefore, conditions leading to decreased renal perfusion and reduced tubular sodium content lead to renin enzyme release into the bloodstream. Negative feedback from humoral factors like angiotensin I, potassium (renin release is increased by hypokalemia and decreased by hyperkalemia), and ANP (atrial natriuretic peptide)
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