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  • Title: Dissociation of colonic apical Na/H exchange activity from bulk cytoplasmic pH.
    Author: Dagher PC, Behm T, Taglietta-Kohlbrecher A, Egnor RW, Charney AN.
    Journal: Am J Physiol; 1996 Jun; 270(6 Pt 1):C1799-806. PubMed ID: 8764164.
    Abstract:
    Intracellular acidification by stimuli rather than CO2 fails to stimulate colonic apical Na/H ex-change and Na absorption. We examined whether Na absorption could be stimulated in the absence of changes in cytoplasmic pH (pHi). Distal colon of male Sprague-Dawley rats was used for pHi measurements with 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein and for flux measurements in Ussing chambers. In 21 mM HCO3-Ringer, increasing PCO2 from 20 to 70 mmHg decreased pHi from 7.51 to 7.03 and increased net Na flux (JnetNa) from 4.2 +/- 0.4 to 6.8 +/- 0.6 mu eq.cm-2.h-1. Similar increases in JnetNa occurred in the absence of mucosal CI and in the presence of phalloidin to inhibit microfilaments or penzolamide to inhibit membrane-bound carbonic anhydrase. sohydric increases in Pco2 did not alter pHi but stimulated JnetNa from 5.1 +/- 0.6 to 7.2 +/- 0.8 mu eq.cm-2.h-1. Carbonyl cyanide m-chlorophenylhydrazone (CCCP) decreased pHi from 7.45 to 7.35 but did not stimulate JnetNa. Butyrate (25 mM) decreased pHi from 7.15 to 7.02 with recovery to baseline within 6 min; however, JnetNa increased by 2.2 mu eq.cm-2.h-1 for 60 min. We conclude that apical Na/H exchange activity is unresponsive to changes in bulk pHi and is independent of Cl/HCO3 exchange, microfilaments, and membrane-bound carbonic anhydrase. The presence of an H-tight, CO2, and butyrate-permeable subapical domain is postulated.
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