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Aldosterone is the primary of several endogenous members of the class of mineralocorticoids in human. Deoxycorticosterone is another important member of this class. Aldosterone tends to promote Na+ and water retention, and lower plasma K+ concentration by the following mechanisms:

  1. Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it up regulates and activates the basolateral Na+/K+ pumps, stimulating ATP hydrolysis leading to phosphorylation of the pump and a conformational change in the pump exposes the Na+ ions to the outside. The phosphorylated form of the pump has a low affinity for Na+ ions, hence reabsorbing sodium (Na+) ions and water into the blood, and secreting potassium (K+) ions into the urine.
  2. Aldosterone up regulates epithelial sodium channel (ENaC) increasing apical membrane permeability for Na+.
  3. Cl- is reabsorbed in conjunction with sodium cations to maintain the system's electrochemical balance.
  4. Aldosterone stimulates uptake of K+ into cells.
  5. Aldosterone stimulates Na+ and water reabsorption from the gut salivary and sweat glands in exchange for K+.
  6. Aldosterone stimulates H+ secretion by intercalated cells in the collecting duct, regulating plasma bicarbonate (HCO3−) levels and its acid/base balance.[4]
  7. Aldosterone may act on the central nervous system via the posterior pituitary gland to release vasopressin (ADH), which serves to conserve water by direct actions on renal tubular reabsorption.[citation needed]

Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal GFR (glomerular filtration rate).[5]

Aldosterone, most probably acting through mineralocorticoid receptors, may positively influence neurogenesis in the dentate gyrus. [6]

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