Figure 214

Na+-Cl- cotransport in distal convoluted tubules. This transport protein, shown by the open circle on the apical cell membrane, does not require K+ for its function. It is a different gene product than the Na+-K+-2Cl~cotransporter. Na+-Cl~cotransport is limited largely, if not entirely, to the distal convoluted tubules.

tion (reabsorptive or secretory) and magnitude of K+ transport is governed by the metabolic state of the individual, the amount and rate of Na+ and fluid flow through the distal convoluted tubule, and the action of aldosterone. As noted earlier, the main source of urinary K+ is tubular secretion by distal convoluted tubules and collecting ducts. K+ secretion also increases during alkalosis and with elevated dietary K+ intake. Increases in the rate or amount of Na+ absorption or of the rate of fluid flow through the distal convoluted tubule stimulate K+ secretion into the tubular fluid. These observations are especially important because they account for the elevated K+ losses that attend the use of diuretics acting in more proximate segments, such as thick ascending limbs and distal convoluted tubules.

In distal convoluted tubules, calcium is transported by an active transport mechanism through rather than between cells. Moreover, in distal convoluted tubules there is a reciprocal relation between the direction and magnitude of calcium on Na+ transport. As Na+ absorption increases, calcium decreases, and conversely, reductions of Na+ absorption are accompanied by elevated calcium reabsorption. This interaction has important implications for diuretics acting in the distal convoluted tubule.

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