Evidence for cl--independent hco3-transport in basolateral
membranes of oxyntopeptic cells of necturus gastric mucosa.
Klingensmith, Mary E., Robert R. Cima, Audrey E. Gadacz, and David I.
Soybel.
Department of Surgery, Brigham and Women's Hospital, Harvard
Medical School, Boston, Massachusetts, 02115
APStracts 3:0149G, 1996.
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. Based on 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 (BCECF) to evaluate Cl-
-independent HCO3- transport across the basolateral membranes of
intact oxyntopeptic cells. Removal of serosal Cl- increased 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,
DIDS, and 0 HCO3-/HEPES 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 which 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.
Received 19 April 1996; accepted in final form 26 July 1996.
APS Manuscript Number G144-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996