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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).
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.
However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of these cells provides a platform for the production of a recurrent Ca 2+ channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major ...
One cause of this can be increased renin production due to narrowing of the renal artery, or a juxtaglomerular cell tumor that produces renin. These will lead to secondary hyperaldosteronism, which will cause hypertension, high blood sodium, low blood potassium, and metabolic alkalosis. [citation needed]
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]
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.
When renal blood flow is reduced (indicating hypotension) or there is a decrease in sodium or chloride ion concentration, the macula densa of the distal tubule releases prostaglandins (mainly PGI2 and PGE2) and nitric oxide, which cause the juxtaglomerular cells lining the afferent arterioles to release renin, activating the renin–angiotensin–aldosterone system, to increase blood pressure ...