Effect of luminal chloride on cell pH in rabbit proximal tubule

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Abstract

The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 ± 0.06 to 7.52 ± 0.06, P < 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 ± 0.06 to 7.60 ± 0.05, P < 0.05), a much greater cel aidification was observed in the presence of 1 mM formate (7.69 ± 0.05 to 7.58 ± 0.06, P < 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume254
Issue number5
StatePublished - 1988

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formic acid
Chlorides
Rabbits
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Sodium-Hydrogen Antiporter
Membranes
Amiloride
Bicarbonates

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Effect of luminal chloride on cell pH in rabbit proximal tubule",
abstract = "The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 ± 0.06 to 7.52 ± 0.06, P < 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 ± 0.06 to 7.60 ± 0.05, P < 0.05), a much greater cel aidification was observed in the presence of 1 mM formate (7.69 ± 0.05 to 7.58 ± 0.06, P < 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange.",
author = "M. Baum",
year = "1988",
language = "English (US)",
volume = "254",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
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T1 - Effect of luminal chloride on cell pH in rabbit proximal tubule

AU - Baum, M.

PY - 1988

Y1 - 1988

N2 - The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 ± 0.06 to 7.52 ± 0.06, P < 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 ± 0.06 to 7.60 ± 0.05, P < 0.05), a much greater cel aidification was observed in the presence of 1 mM formate (7.69 ± 0.05 to 7.58 ± 0.06, P < 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange.

AB - The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 ± 0.06 to 7.52 ± 0.06, P < 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 ± 0.06 to 7.60 ± 0.05, P < 0.05), a much greater cel aidification was observed in the presence of 1 mM formate (7.69 ± 0.05 to 7.58 ± 0.06, P < 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange.

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