AJP - Gastrointestinal and Liver Physiology, Vol 239, Issue 6 536-G542, Copyright © 1980 by American Physiological Society
Role of nutrient HCO3(-) in protection of amphibian gastric mucosa
R. Schiessel, A. Merhav, J. B. Matthews, L. A. Fleischer, A. Barzilai and W. Silen
In in vitro bullfrog fundic mucosa inhibited with 10(-3) M metiamide and
exposed to a luminal pH of 2 a progressive slow decline in potential
difference (PD) and short-circuit current (Isc) and a rise in resistance
(R) were observed when the nutrient solution (N) contained 18 mM HCO3(-),
but these changes were restored by an N containing 50 mM HCO3(-).
Substitution of PO4(3-) or
N-tris(hydroxymethyl)-methyl-2-aminoethanesulfonic acid for NHO3(-) in N
caused a rapid drop in PD and Isc in inhibited tissues, changes that could
be prevented by 10(-4) M histamine. Ulceration occurred more frequently in
metiamide-inhibited gastric sacs exposed to artificial gastric juice with
an N of 18 mMHCO3(-) than with 50 mM HCO3(-), but histamine prevented
ulceration in the 18 mM HCO3(-) solution. JnetCl approximated Isc under
most experimental conditions in inhibited mucosa and was reduced
dramatically as were both Jn leads to sCl and Js leads to nCl when HCO3(-)
was removed from N. In histamine-stimulated tissues, removal of nutrient
HCO3(-) did not influence Cl- transport. Our results are consistent with
the proposal that HCO3(-) in N supports normal Cl- flux and that the
alkaline tide of actively secreting oxyntic cells can do the same in the
absence of ambient HCO3(-).
