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Aldosterone release causes sodium and water retention, which causes increased blood volume, and a subsequent increase in blood pressure, which is sensed by the baroreceptors. [39] To maintain normal homeostasis these receptors also detect low blood pressure or low blood volume, causing aldosterone to be released.
The name mineralocorticoid derives from early observations that these hormones were involved in the retention of sodium, a mineral.The primary endogenous mineralocorticoid is aldosterone, although a number of other endogenous hormones (including progesterone [1] and deoxycorticosterone) have mineralocorticoid function.
by the stretch receptors located in the atria of the heart. by adrenoglomerulotropin, a lipid factor, obtained from pineal extracts. 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 ...
The mineralocorticoid receptor (or MR, MLR, MCR), also known as the aldosterone receptor or nuclear receptor subfamily 3, group C, member 2, (NR3C2) is a protein that in humans is encoded by the NR3C2 gene that is located on chromosome 4q31.1-31.2. [5] MR is a receptor with equal affinity for mineralocorticoids and glucocorticoids.
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).
Kisspeptin directly increases release of aldosterone by several means, the first being through these receptors leading to a direct route to aldosterone release. [24] Secondly, the H295R adrenal cells stimulated by kisspeptin can synthesize aldosterone by breaking down pregnenolone more efficiently. [24]
In the adrenal cortex, angiotensin II acts to cause the release of aldosterone. Aldosterone acts on the tubules (e.g., the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. This increases blood volume and, therefore, increases blood pressure.
This causes the release of aldosterone into the blood. Aldosterone acts primarily on the distal convoluted tubules and collecting ducts of the kidneys, stimulating the excretion of potassium ions into the urine. [64] It does so, however, by activating the basolateral Na + /K + pumps of the tubular epithelial cells. These sodium/potassium ...