Effect of atropine on pancreatic response to HCl and secretin

Abstract

In dogs with gastric and pancreatic fistulas, the effect of atropine was studied on the pancreatic secretory response to secretin and intestinal HCl. Atropine sulfate (20 .mu.g.cntdot.kg-1.cntdot.h-1 iv) significantly depressed basal HCO3- and protein output. Atropine depressed HCO3- responses to low doses (62.5, 125, 250 and 500 ng.cntdot.kg-1.cntdot.h-1) of secretin but had no significant effect on responses to high doses (1000 and 2000 ng.cntdot.kg-1.cntdot.h-1). Secretin, with or without atropine, did not stimulate pancreatic protein output above basal. Atropine depressed HCO3- responses to low loads (3, 6 and 12 mmol.cntdot.h-1) of HCl but had no significant effect on responses to high loads (12, 24 and 48 mmol.cntdot.h-1). Intraduodental HCl produced a dose-dependent increase in protein output. Atropine abolished protein responses to low loads (3 and 6 mmol.cntdot.h-1) but did not affect responses to high loads (24 and 48 mmol.cntdot.h-1) of HCl. These findings are compatible with the hypotheses that endogenous cholinergic activity augments the pancreatic HCO3- response to secretin and that the pancreatic protein response to intraduodental HCl is, at least in part, mediated cholinergically.