The present in vitro microperfusion study examined whether active NaCl transport in the proximal convoluted tubule (PCT) occurs via parallel Na+-H+ and Cl--HCO3 -(OH-) exchangers. PCT were perfused with a high chloride, low-bicarbonate solution simulating late proximal tubular fluid, and were bathed in a similar solution containing 6 g/dl albumin. In this setting the driving forces responsible for passive NaCl transport are eliminated. Addition of 0.1 or 0.5 mM luminal 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), 0.5 mM luminal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), or 0.1 mM bath ethoxyzolamide, a lipophilic carbonic anhydrase inhibitor, resulted in an approximately 50% reduction in volume absorption. Inhibition of the Na+-H+ antiporter with 1.0 mM luminal amiloride inhibited volume absorption by 50%. The transepithelial potential difference (PD) was no significantly different from zero, consistent with an electroneutral mechanism for active NaCl transport. The effect of a Cl--HCO3 -(OH-) exchanger on acidification was examined in PCT perfused with an ultrafiltrate-like solution and bathed in a serumlike albumin solution. Addition of 0.5 mM DIDS did not significantly decrease volume absorption, demonstrating that luminal DIDS did not result in a nonspecific decrease in solute transport. Luminal DIDS significantly stimulated bicarbonate absorption, consistent with a Na+-H+ antiporter running in parallel with a Cl--HCO3 -(OH-) antiporter, which exchanges luminal Cl- for cellular HCO3 - (or OH-). In conclusion, these data are consistent with parallel Na+-H+ and Cl--HCO3 -(OH-) antiporters mediating neutral active NaCl transport in the PCT.
|Original language||English (US)|
|Title of host publication||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - 1987|
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