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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 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).
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.
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.
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.
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]
Angiotensin II exerts system wide effects, triggering aldosterone release from the adrenal cortex, direct vasoconstriction, and thirst behaviors originating in the hypothalamus. This is commonly known as the renin-angiotensin-aldosterone system.
The immune system specifically targets the cells of the adrenal cortex and destroys them, but Addison's disease can also be caused by a severe infection such as tuberculosis. Some symptoms include hypoglycemia and decreased blood sodium levels and increased blood potassium levels caused by a deficiency of aldosterone. These electrolyte ...