Captopril inhibits secretin-induced pancreatic bicarbonate output

Renin-angiotensin systems function at both the organ and systemic levels. Previous studies suggest that angiotensin II (Ang II) stimulates pancreatic secretion in vitro. In contrast, in vivo studies suggest that Ang II inhibits pancreatic secretion. To further assess Ang II's influence on pancreatic secretion, we examined the effect of captopril on secretin-stimulated pancreatic output.

After a 30-min basal period, four conscious dogs with chronic gastric and Herrera pancreatic fistulas received an intravenous bolus of captopril (0.1 mg/kg) followed by a continuous infusion (25 microg/kg/min). Control studies were performed with volume- and rate-matched saline infusion. After 1 h, secretin infusion was begun at 16 ng/kg/h, doubling the dose every 30 min. Pancreatic juice was analyzed for bicarbonate and protein. A paired t test was used to assess statistical significance.

When compared to controls, pancreatic bicarbonate outputs were lower during captopril administration; the difference between captopril and control was statistically significant at the highest secretin dose. Protein outputs also appeared lower during captopril administration, although these differences were not statistically significant.

These data suggest that Ang II may augment secretin-induced pancreatic secretion. Further, the data seemingly refute the inhibitory role attributed to Ang II in earlier studies.