AJP - Gastrointestinal and Liver Physiology, Vol 239, Issue 6 485-G492, Copyright © 1980 by American Physiological Society
Secretion of H+ and K+ by bullfrog gastric mucosa: characterization of K+ transport pathway
P. C. Sen, L. L. Tague and T. K. Ray
The transport of K+ and H+ (both expressed as mueq/h) by in vitro chambered
bullfrog (Rana catesbeiana) gastric mucosa have been studied under a
variety of conditions such as anoxia, addition of p-chloromercuribenzene
sulfonic acid (PCMBS) into the secretory solution, inclusion of ouabain in
the nutrient solution, addition of thiocyanate (SCN-) into the mucosal
solution, and replacement of nutrient chloride (Cl-) with sulfate
(SO4(2-)), or gluconate (Gl). Anoxia reversibly reduced the H+ transport
close to zero within 15 min and gradually reduces the K+ transport
throughout the 2-h period of anoxia. The presence of 2.5 X 10(-4) M mucosal
PCMBS in the histamine-stimulated mucosa increases the K+ transport, which
is promptly reduced by changing the gas phase to 95% N2-5% CO2. Addition of
ouabain to the nutrient solution of the histamine-stimulated mucosa with
PCMBS on the mucosal side significantly (P < 0.05) reduces the K+
transport within 60 min. Addition of SCN- to the mucosal solution of a
histamine-stimulated mucosa with regular nutrient or O, K+ nutrient and 10,
K+ mucosal solution reduces the H+ transport to near zero within 60 min.
This SCN- inhibition can be reversed by elevating secretory K+.
Substitution of nutrient Cl- with SO4(2-) or Gl in the histamine-stimulated
mucosa reversibly inhibits H+ transport and reduces K+ transport to a low
level (0.7 +/- 0.05). Our data suggest that the K+ transport across the
apical membranes of gastric cells is to a large extent a passive
carrier-mediated process, and the transport of both K+ and Cl- are coupled
at the apical membrane.
