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.