Principal and intercalated cells of the collecting ducts. Principal (top) cells reabsorb Na+ and the secreted K+. Na+ entry across apical cell membranes is mediated by a Na+ channel. Na+ exit across basolateral cell membranes is effected by the Na+/K+-ATPase, shown by the filled circle in the principal cell. The rates of Na+ reabsorption and K+ secretion are regulated by aldosterone. Intercalated (bottom) cells reabsorb K+ and HCO3~and secretes H+. K+ entry and H+ secretion are mediated by an H+/K+ ATPase, which is shown by the filled circle in the apical cell membrane of the intercalated cell.
little net K+ transport occurs under K+-replete conditions.
Aldosterone stimulates the rates of Na+ reabsorption and K+ secretion. This is relevant to the action of spironolactone, a diuretic that is a competitive inhibitor of aldosterone (discussed later). It is also pertinent because administration of diuretics can cause secondary hyperaldosteronism, which may exaggerate the potassium wasting that is a consequence of the increased delivery of Na+ and enhanced flow through distal convoluted tubules and collecting ducts.
ADH can significantly modify the total urine volume along with its solute concentration. In the absence of ADH, the collecting ducts are essentially impermeable to water. Little fluid is reabsorbed, and the final urine is dilute with respect to plasma. In other words, the clearance of solute-free water (CH2O) is greater than the os-molar clearance (Cosm). ADH increases water permeability, allowing reabsorption of fluid from the tubules into the interstitium. The driving force for water transport is the osmotic gradient between the medullary in-terstitium and the tubular fluid. NaCl and urea are the two major solutes accounting for the hypertonicity. The NaCl in the interstitium results from the reabsorption of
Na+ by thick ascending limbs. Thus, in the absence of ADH, Na+ reabsorption contributes to medullary interstitial hypertonicity, water abstraction from the collecting ducts, and the formation of concentrated urine. Diuretics blocking Na+ reabsorption by thick ascending limbs will therefore attenuate the formation of dilute urine (CH2O) in hypotonic states when ADH is absent or low. Conversely, in hypertonic conditions, when ADH levels are high and diuretics are blocking Na+ reabsorption by the thick ascending limbs, the generation of concentrated urine is reduced, and Cosm is greater than CH2O.
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