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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.
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.
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]
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 .
Get ready for all of today's NYT 'Connections’ hints and answers for #550 on Thursday, December 12, 2024. Today's NYT Connections puzzle for Thursday, December 12, 2024The New York Times.
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.
On one hand, mutations on the gene NR3C2 (coding the mineralocorticoid receptor) cause the synthesis of a non-functional receptor which is unable to bind aldosterone or function correctly. In the kidney, aldosterone plays an important role of regulating sodium and potassium homeostasis by its actions on distal nephron cells. [3]