The principal role of mineralocorticoids is the regulation of Na+ and K+ excretion. Mineralocorticoids increase the reabsorption of Na+ from the urine, sweat, saliva, and gastric juice. Sodium ions move out of urine (and other transcellular fluids) into the interstitial fluid where they are retained so that the ECF concentration of Na+ increases.
The actions of aldosterone are localized to the distal tubular and collecting duct cells of the kidney, (i) Aldosterone increases reabsorption of Na+ and with it, of water too. (ii) Increased Na+ reabsorption makes the tubular lumen highly negative, (iii) The highly negative lumen together with the increased apical permeability to K+ promotes K+ secretion.
Aldosterone is the sole regulator of the external potassium balance. An increase in plasma K+ stimulates aldosterone secretion, which in turn restores plasma K+ levels by promoting kaliuresis. An absence of this aldosterone-feedback mechanism would result in fatal hyperkalemia. Aldosterone is one of the several regulators of body Na+ and water balance, another important regulator being the thirst-ADH mechanism.
In the absence of the aldosterone-feedback mechanism, the thirst-ADH mechanism maintains a near-perfect Na+ balance in the body. In the absence of the ADH-thirst mechanism, however, aldosterone is unable to maintain proper Na+ balance because of the escape phenomenon.