aldosteronedependent

Aldosteronedependent describes biological processes, tissues, or disease states that require aldosterone signaling to occur or to progress. Aldosterone is a mineralocorticoid hormone produced by the adrenal cortex, and its effects are primarily mediated through the intracellular mineralocorticoid receptor expressed in principal cells of the kidney’s distal nephron and in other aldosterone-responsive tissues.

In the kidney, aldosterone binds to the mineralocorticoid receptor and induces the transcription of genes such as those encoding the epithelial sodium channel (ENaC) subunits and the Na+/K+ ATPase. This promotes sodium reabsorption, water retention, and potassium secretion, contributing to extracellular fluid volume and blood pressure regulation. Aldosterone also enhances hydrogen ion secretion via H+-ATPase in intercalated cells, influencing acid-base balance. The renin-angiotensin-aldosterone system modulates aldosterone secretion in response to changes in blood pressure, plasma sodium, and potassium levels.

Clinically, the concept of aldosteronedependent is used to describe conditions where aldosterone signaling is a key driver of pathology or treatment response. Primary aldosteronism (hyperaldosteronism) is a classic example, characterized by excess aldosterone production leading to hypertension and hypokalemia. Aldosterone can contribute to cardiac and vascular remodeling with chronic exposure, and it plays a role in some forms of resistant hypertension.

Diagnosis often involves measurements such as the aldosterone-to-renin ratio, with confirmation tests and imaging used as appropriate. Treatments include mineralocorticoid receptor antagonists (e.g., spironolactone, eplerenone) and, in unilateral cases, surgical removal of an aldosterone-producing lesion.