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In the fetus, the renin–angiotensin system is predominantly a sodium-losing system, [citation needed] as angiotensin II has little or no effect on aldosterone levels. Renin levels are high in the fetus, while angiotensin II levels are significantly lower; this is due to the limited pulmonary blood flow, preventing ACE (found predominantly in ...
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 ...
Aldosterone is part of the renin–angiotensin–aldosterone system. It has a plasma half-life of less than 20 minutes. [ 9 ] Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives, like lisinopril , which lowers blood pressure by blocking the angiotensin-converting enzyme (ACE), leading to lower ...
The outermost layer, the zona glomerulosa is the main site for the production of aldosterone, a mineralocorticoid. The synthesis and secretion of aldosterone are mainly regulated by the renin–angiotensin–aldosterone system. The zona glomerulosa cells express a specific enzyme aldosterone synthase (also known as CYP11B2).
In response to increased potassium levels, renin or decreased blood flow to the kidneys, cells of the zona glomerulosa produce and secrete the mineralocorticoid aldosterone into the blood as part of the renin–angiotensin system. [1]
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.
Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle.
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]