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Angiotensin II mediates its physiological effects of vasoconstriction and sodium and water reabsorption through the AT1-R.

It is widely distributed in many cell types, including the heart, vasculature, kidney, adrenal glands, pituitary, and central nervous system. These receptors have different and often opposing physiological responses. The physiological and pathophysiological effects of angiotensin II are mediated by two types of receptors: type 1 and type 2.

Angiotensin II has been implicated in the pathogenesis of hypertension, atherosclerotic disease, heart failure, and kidney disease through these effects. Release of vasopressin from the hypothalamus Īngiotensin II is also implicated in many pathophysiological states and is known to induce oxidative stress, vascular smooth muscle contraction, endothelial dysfunction, fibrosis, and hypertrophic, anti-apoptotic, and pro-mitogenic effects. The physiological effects of angiotensin II on extracellular volume and blood pressure regulation are mediated in five ways: Angiotensin III has been shown to have 100% of the aldosterone-stimulating effect of angiotensin II but 40% of the pressor effects, while angiotensin IV has further decreased the systemic effect. Peptidases degrade it into angiotensin III and IV. 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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