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Aldosterone is the primary of several endogenous members of the class of mineralocorticoids in humans. [citation needed] Deoxycorticosterone is another important member of this class. Aldosterone tends to promote Na + and water retention, and lower plasma K + concentration by the following mechanisms:
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.
In physiology, aldosterone escape is a term that has been used to refer to two distinct phenomena involving aldosterone that are exactly opposite each other: Escape from the sodium -retaining effects of excess aldosterone (or other mineralocorticoids ) in primary hyperaldosteronism , manifested by volume and/or pressure natriuresis .
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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).
Lorundrostat (developmental name MLS 101) is an aldosterone synthase inhibitor developed by Mineralys Therapeutics for high blood pressure. In clinical trials as an add-on medication for people with uncontrolled hypertension, decreased renin and elevated aldosterone it significantly reduced blood pressure. Hyperkalemia occurred in some trial ...
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.
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