Evidence for Cl- -independent HCO3- transport in basolateral membranes of Necturus oxyntopeptic cells

Mary E. Klingensmith, Robert R. Cima, Audrey E. Gadacz, David Soybel

Research output: Contribution to journalArticle

Abstract

Luminal H+ secretion by gastric mucosa is accompanied by basolateral HCO3- release. A basolateral Cl-/HCO3- exchanger is known to mediate HCO3- extrusion from oxyntopeptic cells during resting and secretagogue-induced apical HCl secretion. From recent work, we hypothesized that there might be a Cl--independent pathway for basolateral HCO3- exit in Necturus oxyntopeptic cells. In this study, we used a fluorescent pH indicator [2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein] to evaluate Cl--independent HCO3- transport across the basolateral membranes of intact oxyntopeptic cells. Removal of serosal Cl- increased intracellular pH (pHi) (7.05 to 7.25), consistent with Cl--dependent HCO3- extrusion. Removal of serosal Na+ in the absence of Cl- resulted in significant acidification of pHi (7.10 to 6.89), but studies involving amiloride, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (BIDS), and 0 HCO3--N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid-buffered solutions suggest that Na+-dependent changes in pHi are due to Na+/H+ exchange. Our studies demonstrate a marked concentration-dependent alkalinization when tissues are exposed to increases in serosal K+. A substantial part of this alkalinization in response to increases in serosal K+ (pHi 7.00 to 7.46) appears to be a HCO3- exit pathway that is independent of both Na+ and Cl-, unaffected by bumetanide or amiloride, but sensitive to DIDS. We propose the presence of a Cl-- and Na+-independent K+-dependent HCO3- cotransporter in Necturus oxyntopeptic cell basolateral membranes.

Original languageEnglish (US)
JournalAmerican Journal of Physiology
Volume271
Issue number6 PART 1
StatePublished - Dec 1 1996

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Necturus
Membranes
Chloride-Bicarbonate Antiporters
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Amiloride
Gastric Mucosa
Cell Membrane
Acids

All Science Journal Classification (ASJC) codes

  • Physiology (medical)

Cite this

Klingensmith, Mary E. ; Cima, Robert R. ; Gadacz, Audrey E. ; Soybel, David. / Evidence for Cl- -independent HCO3- transport in basolateral membranes of Necturus oxyntopeptic cells. In: American Journal of Physiology. 1996 ; Vol. 271, No. 6 PART 1.
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abstract = "Luminal H+ secretion by gastric mucosa is accompanied by basolateral HCO3- release. A basolateral Cl-/HCO3- exchanger is known to mediate HCO3- extrusion from oxyntopeptic cells during resting and secretagogue-induced apical HCl secretion. From recent work, we hypothesized that there might be a Cl--independent pathway for basolateral HCO3- exit in Necturus oxyntopeptic cells. In this study, we used a fluorescent pH indicator [2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein] to evaluate Cl--independent HCO3- transport across the basolateral membranes of intact oxyntopeptic cells. Removal of serosal Cl- increased intracellular pH (pHi) (7.05 to 7.25), consistent with Cl--dependent HCO3- extrusion. Removal of serosal Na+ in the absence of Cl- resulted in significant acidification of pHi (7.10 to 6.89), but studies involving amiloride, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (BIDS), and 0 HCO3--N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid-buffered solutions suggest that Na+-dependent changes in pHi are due to Na+/H+ exchange. Our studies demonstrate a marked concentration-dependent alkalinization when tissues are exposed to increases in serosal K+. A substantial part of this alkalinization in response to increases in serosal K+ (pHi 7.00 to 7.46) appears to be a HCO3- exit pathway that is independent of both Na+ and Cl-, unaffected by bumetanide or amiloride, but sensitive to DIDS. We propose the presence of a Cl-- and Na+-independent K+-dependent HCO3- cotransporter in Necturus oxyntopeptic cell basolateral membranes.",
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Evidence for Cl- -independent HCO3- transport in basolateral membranes of Necturus oxyntopeptic cells. / Klingensmith, Mary E.; Cima, Robert R.; Gadacz, Audrey E.; Soybel, David.

In: American Journal of Physiology, Vol. 271, No. 6 PART 1, 01.12.1996.

Research output: Contribution to journalArticle

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AB - Luminal H+ secretion by gastric mucosa is accompanied by basolateral HCO3- release. A basolateral Cl-/HCO3- exchanger is known to mediate HCO3- extrusion from oxyntopeptic cells during resting and secretagogue-induced apical HCl secretion. From recent work, we hypothesized that there might be a Cl--independent pathway for basolateral HCO3- exit in Necturus oxyntopeptic cells. In this study, we used a fluorescent pH indicator [2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein] to evaluate Cl--independent HCO3- transport across the basolateral membranes of intact oxyntopeptic cells. Removal of serosal Cl- increased intracellular pH (pHi) (7.05 to 7.25), consistent with Cl--dependent HCO3- extrusion. Removal of serosal Na+ in the absence of Cl- resulted in significant acidification of pHi (7.10 to 6.89), but studies involving amiloride, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (BIDS), and 0 HCO3--N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid-buffered solutions suggest that Na+-dependent changes in pHi are due to Na+/H+ exchange. Our studies demonstrate a marked concentration-dependent alkalinization when tissues are exposed to increases in serosal K+. A substantial part of this alkalinization in response to increases in serosal K+ (pHi 7.00 to 7.46) appears to be a HCO3- exit pathway that is independent of both Na+ and Cl-, unaffected by bumetanide or amiloride, but sensitive to DIDS. We propose the presence of a Cl-- and Na+-independent K+-dependent HCO3- cotransporter in Necturus oxyntopeptic cell basolateral membranes.

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