Contribution of prostaglandins to dopamine actions in the pancreas of anesthetized dogs

We investigated the effect of dopamine and arachidonic acid on pancreatic blood flow and exocrine secretion in the isolated blood-perfused pancreas of pentobarbital sodium-anesthetized dogs without or with pretreatment with indomethacin or sodium meclofenamate in the absence and during infusion of prostaglandins I2 or E2 (PGI2 or PGE2). Intra-arterial administration of dopamine (50-500 ng/kg) produced an initial vasoconstriction followed by vasodilation and enhanced flow rate of pancreatic exocrine secretion. Arachidonic acid (0.5-5 micrograms/kg) produced vasodilation without altering the flow rate of pancreatic exocrine secretion. In animals pretreated with indomethacin or sodium meclofenamate (10 mg/kg iv), the magnitude and the duration of the biphasic vascular response but not the increase in flow rate of pancreatic exocrine secretion elicited by dopamine were reduced. Arachidonic acid-induced vasodilation was abolished by the cyclooxygenase inhibitors. During infusion of PGI2 or PGE2 (10 ng X kg-1 X min-1 ia), the inhibitory effect of indomethacin or sodium meclofenamate on the vasodilator phase of the response to dopamine was diminished. These data suggest that prostaglandins, presumably PGI2 and PGE2, contribute to the effect of dopamine to increase pancreatic blood flow but not to increase pancreatic exocrine secretion in anesthetized dogs.