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Aldosterone is increased at low sodium intakes, but the rate of increase of plasma aldosterone as potassium rises in the serum is not much lower at high sodium intakes than it is at low. Thus, potassium is strongly regulated at all sodium intakes by aldosterone when the supply of potassium is adequate, which it usually is in hunter-gatherer diets.
Pseudohyperaldosteronism (also pseudoaldosteronism) is a medical condition which mimics the effects of elevated aldosterone (hyperaldosteronism) by presenting with high blood pressure, low blood potassium levels (hypokalemia), metabolic alkalosis, and low levels of plasma renin activity (PRA).
Aldosterone has effects on most or all cells of the body but, clinically, the most important actions are in the kidney, on cells of the late distal convoluted tubule and medullary collecting duct. In the principal cells aldosterone increases activity of basolateral membrane sodium-potassium ATPase and apical epithelial sodium channels, ENaC ...
It regulates pH by absorbing bicarbonate and secreting protons (H +) into the filtrate, or by absorbing protons and secreting bicarbonate into the filtrate. Sodium and potassium levels are controlled by secreting K + and absorbing Na +. Sodium absorption by the distal tubule is mediated by the hormone aldosterone. Aldosterone increases sodium ...
Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the active secretion of potassium in the principal cells of the cortical collecting tubule and active secretion of protons via proton ATPases in the lumenal membrane of the intercalated cells of the collecting tubule.
Aldosterone within the connecting tubule lumen enhances connecting tubule glomerular feedback (CTGF) via a nongenomic effect involving GPR30 receptors and sodium/hydrogen exchanger (NHE). Aldosterone inside the connecting tubule lumen enhances CTGF via a cAMP/PKA/PKC pathway and stimulates O2− generation and this process may contribute to ...
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
Both hormones exert their effects principally on the collecting ducts. Tubular secretion occurs simultaneously during re-absorption of filtrate. Substances, generally produced by body or the by-products of cell metabolism that can become toxic in high concentration, and some drugs (if taken). These all are secreted into the lumen of renal tubule.