MRAldosteronKomplex

The MRAldosteronKomplex refers to the molecular complex formed when aldosterone binds to the mineralocorticoid receptor (MR), a ligand-activated transcription factor of the nuclear receptor family. In many cells, MR is retained in the cytoplasm by chaperone proteins such as HSP90. Aldosterone binding induces a conformational change, releases the chaperones, and promotes MR translocation into the nucleus where it dimerizes and binds to mineralocorticoid response elements in DNA.

Once bound to DNA, the MRAldosteronKomplex recruits transcriptional coactivators and regulates the expression of target genes. Key examples include subunits of the epithelial sodium channel (ENaC) and the Na+/K+-ATPase, as well as the SGK1 kinase, which enhances ENaC activity at the cell surface. The net effect is increased sodium reabsorption and potassium excretion, contributing to fluid balance and blood pressure regulation. Although prominent in the kidney’s distal nephron, MR signaling also influences electrolyte handling in other epithelial tissues such as the colon and sweat glands.

Physiological role and regulation are mediated by the renin-angiotensin-aldosterone system, potassium levels, and tissue-specific expression of the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which protects MR from activation by circulating glucocorticoids. Dysregulation of the MRAldosteronKomplex is associated with conditions like hyperaldosteronism, hypertension, and hypokalemia.

Therapeutically, MR antagonists such as spironolactone and eplerenone inhibit this complex’s action and are used to treat related disorders.