Angiotensin II increases vascular smooth muscle contraction and raises systemic vascular resistance. These effects take place by activation of angiotensin II receptor type I.
Angiotensin II causes widespread vasoconstriction, promotes reabsorption of Na, and increases ADH release. All of these effects together increase blood pressure.
Angiotensin II is a potent vasoconstrictor that preferentially constricts efferent arterioles.This increases GFR even in the cases of decreased renal blood flow (e.g., hypotension).
Even though angiotensin II constricts the afferent arteriole, resulting in decreased renal blood flow, the preferential constriction of the efferent arteriole increases glomerular filtration rate (GFR).
Angiotensin II increases the reabsorption of sodium and water in the proximal convoluted tubule by activating Na/H exchanger.
Activation of Na/H exchanger in the proximal tubule results in sodium reabsorption. This creates a sodium concentration gradient that promotes water reabsorption.
Angiotensin II also acts on the adrenal cortex, where it promotes the synthesis and release of aldosterone.
Angiotensin II promotes the synthesis and release of aldosterone from the adrenal cortex, which increases reabsorption of sodium and water and secretion of potassium by acting on principal cells of collecting duct. Aldosterone also promotes excretion of hydrogen ions by acting on alpha intercalated cells in late distal convoluted tubule and collecting duct.
Angiotensin promotes the release of antidiuretic hormone (ADH) from the posterior pituitary. ADH promotes water reabsorption by increasing aquaporin expression in principal cells of collecting duct.
Angiotensin II also has effects on the hypothalamus. It amplifies the sensation of thirst resulting in increased water intake.
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