Prostacyclin inhibits pancreatic secretion

Abstract

Prostacyclin (PGI2), the major product of arachidonate metabolism in the gastrointestinal tract, was shown to affect gastric blood flow and gastric secretion, but it is unknown whether it also affects pancreatic secretion. This study was designed to determine the influence of PGI2 on pancreatic secretion under basal conditions and in response to exogenous and endogenous stimulants. PGI2 alone given in graded intravenous doses caused a slight pancreatic bicarbonate and protein secretion in fasted dogs. When given during stimulated pancreatic secretion, PGI2 caused a potent inhibition of the bicarbonate and protein secretion induced by feeding a liver meal, by duodenal perfusion with hydrochloric acid or amino acid mixture, and by intravenous infusion of secretin or caerulein. The kinetic analysis showed that the interaction between PGI2 and secretin affecting bicarbonate secretion is of a mixed type (increased half-maximal dose response, decreased calculated maximal response). This indicates that PGI2 decreases both the total secretory capacity of the pancreas to secrete bicarbonate and reduces the sensitivity of the pancreatic secretory cells to secretin. Because PGI2 significantly reduced the arterial blood pressure, its inhibitory effects on pancreatic secretion could be due, at least in part, to the interference of the blood flow to the pancreas.