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Renin cleaves a decapeptide from angiotensinogen, a globular protein. The decapeptide is known as angiotensin I . 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 ...
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 ...
Renin inhibitor is often preceded by direct, called direct renin inhibitor in order to distinguish its mechanism from other renin–angiotensin–aldosterone system-interfering drugs such as angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs) and aldosterone receptor antagonists.
Angiotensinogen is also known as renin substrate. It is cleaved at the N-terminus by renin to result in angiotensin I, which will later be modified to become angiotensin II. [8] [10] This peptide is 485 amino acids long, and 10 N-terminus amino acids are cleaved when renin acts on it. [8] The first 12 amino acids are the most important for ...
Anatomical diagram of the renin–angiotensin system, showing the role of ACE at the lungs [11] ACE is also part of the kinin–kallikrein system where it degrades bradykinin, a potent vasodilator, and other vasoactive peptides. [12] Kininase II is the same as angiotensin-converting enzyme.
Renin release activates RAAS leading to many outcomes including an increased GFR. The critical target of the trans-JGA signaling cascade is the glomerular afferent arteriole; its response consists of an increase in net vasoconstrictor tone resulting in reductions of glomerular capillary pressure (PGC) and glomerular plasma flow.
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 ...
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.