Renal potassium handling. More than half of filtered potassium is passively reabsorbed by the end of the proximal convolted tubule (PCT). Potassium is then added to tubular fluid in the descending limb of Henle's loop (see below). The major site of active potassium reabsorption is the thick ascending limb of the loop of Henle (TAL), so that, by the end of the distal convoluted tubule (DCT), only 10% to 15% of filtered potassium remains in the tubule lumen. Potassium is secreted mainly by the principal cells of the cortical collecting duct (CCD) and outer medullary collecting duct (OMCD). Potassium reabsorption occurs via the intercalated cells of the medullary collecting duct (MCD). Urinary potassium represents the difference between potassium secreted and potassium reabsorbed . During states of total body potassium depletion, potassium reabsorption is enhanced. Reabsorbed potassium initially enters the medullary interstitium, but then it is secreted into the pars recta (PR) and descending limb of the loop of Henle (TDL). The physiologic role of medullary potassium recycling may be to minimize potassium "backleak" out of the collecting tubule lumen or to enhance renal potassium secretion during states of excess total body potassium . The percentage of filtered potassium remaining in the tubule lumen is indicated in the corresponding nephron segment.
Cellular mechanisms of renal potassium transport: proximal tubule and thick ascending limb. A, Proximal tubule potassium reabsorption is closely coupled to proximal sodium and water transport. Potassium is reabsorbed through both paracellular and cellular pathways. Proximal apical potassium channels are normally almost completely closed. The lumen of the proximal tubule is negative in the early proximal tubule and positive in late proximal tubule segments. Potassium transport is not specifically regulated in this portion of the nephron, but net potassium reabsorption is closely coupled to sodium and water reabsorption. B, In the thick ascending limb of Henle's loop, potassium reabsorption proceeds by electroneutral Na+-K+-2Cl- cotransport in the thick ascending limb, the low intracellular sodium and chloride concentrations providing the driving force for transport. In addition, the positive lumen potential allows some portion of luminal potassium to be reabsorbed via paracellular pathways . The apical potassium channel allows potassium recycling and provides substrate to the apical Na+-K+-2Cl- cotransporter . Loop diuretics act by competing for the Cl- site on this carrier.
Cellular mechanisms of renal potassium transport: cortical collecting tubule. A, Principal cells of the cortical collecting duct: apical sodium channels play a key role in potassium secretion by increasing the intracellular sodium available to Na+-K+-ATPase pumps and by creating a favorable electrical potential for potassium secretion. Basolateral Na+-K+-ATPase creates a favorable concentration gradient for passive diffusion of potassium from cell to lumen through potassium-selective channels. B, Intercalated cells. Under conditions of potassium depletion, the cortical collecting duct becomes a site for net potassium reabsorption. The H+-K+-ATPase pump is regulated by potassium intake. Decreases in total body potassium increase pump activity, resulting in enhanced potassium reabsorption. This pump may be partly responsible for the maintenance of metabolic alkalosis in conditions of potassium depletion .
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