Permissive role of prostaglandins in the action of bradykinin on the pancreas of anesthetized dogs.

We have investigated the contribution of prostaglandins (PGs) to the effect of bradykinin on pancreatic blood flow and pancreatic exocrine secretion by examining its actions in the isolated blood-perfused pancreas of pentobarbital-anesthetized dogs. Intra-arterial injections of bradykinin (0.05-5 ng/kg) into the pancreas produced a dose-dependent vasodilation and increased pancreatic blood flow; the rate of flow, bicarbonate concentration, protein content or pH of the pancreatic juice was not altered. Administration of arachidonic acid (0.5-5 micrograms/kg) into the pancreas also produced vasodilation without altering pancreatic exocrine secretion. In animals pretreated with indomethacin or sodium meclofenamate (10 mg/kg i.v.), the vasodilator effect of bradykinin was attenuated, whereas that of arachidonic acid was abolished; the pancreatic exocrine secretion was not altered. The vasodilation produced by sodium nitroprusside (0.3 micrograms/kg i.a.) in the pancreas was not altered by indomethacin. During infusion of PGI2 or PGE2 (10 ng/kg/min i.a.), the effect of indomethacin or sodium meclofenamate to attentuate bradykinin-induced vasodilation was reduced. However, the sodium nitroprusside-induced vasodilation in animals treated with indomethacin was not altered during infusion of PGI2 or PGE2. These data indicate that PGs, presumably PGI2 and PGE2, play a permissive role in the vasodilator effect of bradykinin in the pancreas of anesthetized dogs. Moreover, these studies suggest that neither bradykinin nor PGs contribute to the regulation of pancreatic exocrine secretion.