Bicarbonate transport in collecting duct segments during chloride-depletion alkalosis.

Abstract

Renal correction of chloride-depletion alkalosis (CDA) by chloride replacement results in bicarbonate secretion in the cortical collecting duct (CD) and urinary bicarbonate excretion. To assess the participation of the more distal segments of the CD, we determined net total CO2 transport in the outer medullary (OMCD), initial (IMCDi) and terminal (IMCDt) inner medullary CD segments obtained from Sprague-Dawley rats with normal acid-base balance (NML) or with CDA produced by peritoneal dialysis. Tubules were bathed and perfused with isotonic solutions containing Cl 110 mM and HCO, 25 mM. Net total CO2 transport was decreased in all segments: OMCD 22.1 +/- 4.2 to 9.2 +/- 2.0; IMCDi 38.1 +/- 4.6 to 9.3 +/- 1.7; IMCDt 6.7 +/- 1.2 to -0.5 +/- 0.4 pmol/min/mm tubule length. Perfusion rates, tubule lengths, and transepithelial voltages did not differ between groups in any segment. These data show that all CD segments beyond the cortical segment decrease bicarbonate reabsorption during CDA. This permits the bicarbonate secreted by the cortical CD to be excreted, and is likely an important mechanism for the correction of CDA.