Search results
Results From The WOW.Com Content Network
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.
Angiotensin I is then converted to an octapeptide, angiotensin II by angiotensin-converting enzyme (ACE), [9] which is thought to be found mainly in endothelial cells of the capillaries throughout the body, within the lungs and the epithelial cells of the kidneys. One study in 1992 found ACE in all blood vessel endothelial cells.
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]
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).
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.
Angiotensin II is a potent pressor hormone and a primary regulator of aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system. It is an important effector controlling blood pressure and volume in the cardiovascular system.
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.
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.