AJP - Gastrointestinal and Liver Physiology, Vol 245, Issue 6 739-G744, Copyright © 1983 by American Physiological Society
Effects of KCl and insulin on benzimidazole-inhibited canine gastric secretion
B. I. Hirschowitz and J. Fong
The final step in acid secretion is believed to result from the
H+-K+-ATPase-mediated exchange of H+ in the parietal cell, with K+ in the
lumen. To study the K+ secretion we used Picoprazole and insulin separately
and together to inhibit gastric secretion stimulated in gastric fistula
dogs with histamine (100 micrograms X kg-1 X h-1). Picoprazole, a
substituted benzimidazole (750 mg/kg), reduced gastric H+ concentration and
volume with a rise in K+ concentration [( K+]) to 20-25 meq/l. Insulin
alone inhibited acid output to the same extent as Picoprazole but with a
marked fall in [K+]. Insulin (0.6 U/kg) given with Picoprazole did not
alter inhibition of H+ but prevented the large decrease in gastric juice
[K+]. An injection of KCl (1 meq/kg) 1 h after Picoprazole did not alter
the effects of the inhibitor. Pepsin secretion after insulin was delayed by
Picoprazole, whereas during bethanechol chloride infusion (80 micrograms X
kg-1 X h-1) pepsin output was reduced for a shorter period and to a lesser
extent than acid. We concluded that insulin affects gastric H+ and K+
secretion by a mechanism not related to H+-K+-ATPase and that Picoprazole
affects pepsin secretion probably indirectly via its effect on the parietal
cell, where its action is quite consistent with an effect limited to
inhibition of the H+-K+-ATPase of the parietal cell.
