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Angiotensin II is the major bioactive product of the renin–angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them; and to receptors on the zona glomerulosa cells, causing the release of aldosterone from the zona glomerulosa in the adrenal cortex.
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).
Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II. Therefore, ACE indirectly increases blood pressure by causing blood ...
Renin (etymology and pronunciation), also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)—also known as the renin-angiotensin-aldosterone axis—that increases the volume of extracellular fluid (blood plasma, lymph, and interstitial fluid) and causes arterial ...
The angiotensin II receptors, (ATR1) and (ATR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. [1] They are important in the renin–angiotensin system : they are responsible for the signal transduction of the vasoconstricting stimulus of the main effector hormone, angiotensin II .
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]
This phenomenon is primarily regulated by the contraction of smooth muscle cells within the vessel walls. Several factors contribute to vasoconstriction, including the release of vasoconstrictor substances such as endothelin and angiotensin II, both of which play crucial roles in the modulation of vascular tone. [16]
They do break up, but they form bundles of vessels (arteriolae recti) that cross the outer zone of the medulla to perfuse the inner zone. Vessels returning from the inner medulla ( venulae recti ) intersperse themselves in a highly regular fashion among the descending arteriolae recti to form a well-organized rete mirabile .