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The epithelial sodium channel (ENaC), (also known as amiloride-sensitive sodium channel) is a membrane-bound ion channel that is selectively permeable to sodium ions (Na +).It is assembled as a heterotrimer composed of three homologous subunits α or δ, β, and γ, [2] These subunits are encoded by four genes: SCNN1A, SCNN1B, SCNN1G, and SCNN1D.
[1] Measuring aldosterone alone is not considered adequate to diagnose primary hyperaldosteronism. Rather, both renin and aldosterone are measured, and a resultant aldosterone-to-renin ratio (ARR) is used for case detection. [20] [21] A high aldosterone-to-renin ratio suggests the presence of primary hyperaldosteronism. The diagnosis is made by ...
The inactivating mutation leads to elevated local concentrations of cortisol in the aldosterone sensitive tissues like the kidney. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor due to the non-selectivity of the receptor, leading to aldosterone-like effects in the kidney.
A mineralocorticoid receptor antagonist (MRA or MCRA) [1] or aldosterone antagonist, is a diuretic drug which antagonizes the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy, in combination with other drugs, for the management of chronic heart failure .
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 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.
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.
Pseudohypoaldosteronism type 1 (PHA1) is characterized by the body's inability to respond adequately to aldosterone, a hormone crucial for regulating electrolyte levels. This condition often manifests with dehydration as the kidneys struggle to retain sufficient salt, leading to symptoms like increased thirst and dry mouth.