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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 ...
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 ...
Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. [ 4 ] [ 5 ] It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. [ 6 ]
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).
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.
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 ...
Aldosterone insufficiency in salt-wasting CAH results in a significant loss of sodium in the urine. Urinary sodium concentrations may exceed 50 mEq/L. Due to the loss of salt at that rate, the infant is unable to maintain proper blood volume and begins to suffer from dehydration due to hyponatremia by the end of the first week of life.
It selectively stimulates secretion of aldosterone. The secretion of aldosterone has a diurnal rhythm. Control of aldosterone release from the adrenal cortex: [citation needed] The role of the renin–angiotensin system: Angiotensin is involved in regulating aldosterone and is the core regulator. Angiotensin II acts synergistically with potassium.