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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.
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.
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 .
Aldosterone stimulates Na + and water reabsorption from the gut, salivary and sweat glands in exchange for K +. Aldosterone stimulates secretion of H + via the H+/ATPase in the intercalated cells of the cortical collecting tubules; Aldosterone upregulates expression of NCC in the distal convoluted tubule chronically and its activity acutely. [18]
ENaC is assembled as a heterotrimer composed of three homologous subunits α, β, and γ or δ, β, and γ. The other ENAC subunits are encoded by SCNN1A, SCNN1G, and SCNN1D. [5] ENaC is expressed in epithelial cells [5] and is different from the voltage-gated sodium channel that is involved in the generation of action potentials in neurons ...
Membrane mineralocorticoid receptors (mMRs) or membrane aldosterone receptors are a group of receptors which bind and are activated by mineralocorticoids such as aldosterone. [ 1 ] [ 2 ] Unlike the classical nuclear mineralocorticoid receptor (MR), which mediates its effects via genomic mechanisms, mMRs are cell surface receptors which rapidly ...
It uses Na-H antiport, Na-glucose symport, sodium ion channels (minor). [1] It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide. It is very efficient, since more than 25,000 mmol/day of sodium is filtered into the nephron, but only ~100 mmol/day, or less than 0.4% remains in the final urine.
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.
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