AJP - Gastrointestinal and Liver Physiology, Vol 248, Issue 1 110-G117, Copyright © 1985 by American Physiological Society
Contribution of prostaglandins to dopamine actions in the pancreas of anesthetized dogs
K. Iwatsuki, T. Homma and K. U. Malik
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.
