Aldosterone Enhances Sodium Reabsorption and Potassium Secretion
Aldosterone is a mineralocorticoid hormone that is secreted by the adrenal cortex. Aldosterone release is stimulated by systemic hypotension through the renin-angiotensin system.
Aldosterone acts on connecting segment cells and the principal cells of the collecting duct to enhance Na+ reabsorption, which in turn enhances water reabsorption to correct perceived volume depletion. At the cellular level, aldosterone increases the permeability of the apical plasma membrane Na4 channels and stimulates Na+,Kf-ATPase activity, thereby enhancing Na+ reabsorption. Chronic aldosterone stimulation even causes a structural adaptation in these cells, the proliferation of the basolateral plasma membrane, where Nat,K+-ATPase resides. In addition, chronic aldosterone stimulation increases transcription of the apical NaCl co-transporter in the distal convoluted tubule and the epithelial Na+ channel (ENaC) in the collecting duct and trafficking of these transport proteins to the apical plasma membrane.Aldosterone release is also stimulated by hyperkalemia (elevated plasma K4 level) and has an important role in regulating K4 homeostasis. The acute effect of aldosterone on K4 is to enhance its entry into aldosterone-responsive cells by stimulating Na4,K4-ATPase activity; this lowers serum K’ levels but has little effect on renal K, excretion. More chronic aldosterone stimulation increases the number of K4 channels in the apical plasma membrane of connecting segment cells and principal cells, thereby increasing the apical K4 permeability and K4 secretion. Therefore the immediate effect of aldosterone is a redistribution of Kt from extracellular to intracellular compartments, but with continued aldosterone stimulation, renal elimination of K4 is augmented.