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Angiotensin II has a variety of effects on the body: [citation needed] Throughout the body, angiotensin II is a potent vasoconstrictor of arterioles. In the kidneys, angiotensin II constricts glomerular arterioles, having a greater effect on efferent arterioles than afferent.
Schematic diagram of the renin–angiotensin–aldosterone system. Angiotensin II is a potent vasoconstrictor in a substrate concentration-dependent manner. [10] Angiotensin II binds to the type 1 angiotensin II receptor (AT1), which sets off a number of actions that result in vasoconstriction and therefore increased blood pressure.
ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction).
Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride , thereby expanding the extracellular fluid compartment and raising blood pressure.
When angiotensin II levels are increased due to activation of the renin–angiotensin–aldosterone system, most of the arteries in the body experience vasoconstriction, in order to maintain adequate blood pressure. However, this reduces blood flow to the kidneys.
The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to G q/11 and G i/o and thus activates phospholipase C and increases the cytosolic Ca 2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C.
The resulting cleaved protein is known as soluble ACE2 or sACE2. It is released into the bloodstream where one of sACE2's functions is to turn excess angiotensin II into angiotensin 1-7 which binds to MasR receptors creating localized vasodilation and hence decreasing blood pressure. Excess sACE2 may ultimately be excreted in the urine. [18] [19]
Once in the bloodstream, renin converts angiotensinogen to angiotensin I. Angiotensin I is further cleaved by the angiotensin-converting enzyme to angiotensin II, which is a potent vasoconstrictor that increases blood pressure. [144] In addition to angiotensin II, other biologically active substances can be formed in mammals.