In vitro stimulation of prostaglandin synthesis in the rat pancreas by carbamylcholine, caerulein and secretin.

Rat pancreas pieces spontaneously released PGE2 (2.3 ng/100 mg x 45 min) and PGF2 alpha (7.6 ng/100 mg x 45 min). This release corresponds probably to a neo-synthesis since it was abolished by indomethacin. Carbamylcholine (greater than or equal to 10 microM), caerulein (greater than or equal to 10 nM) and secretin (greater than or equal to 10 nM) stimulated the release of PGE2 and PGF2 alpha: the concentrations of stimulators required to increase PGs release were thus much higher than those which trigger enzyme secretion. Atropine specifically inhibited the cholinergic stimulation, whereas indomethacin blocked the stimulatory effects of all secretagogues. Stimulation of PGE2 and PGF2 alpha release was reduced in a Ca++-free medium, abolished by EGTA and mimicked by the ionophore A23187, underscoring the crucial role of Ca++ in the regulation of PGs synthesis by the pancreas. Neither PGE2 nor PGF2 alpha stimulated enzyme secretion in this system and indomethacin did not inhibit the secretory effect of carbamylcholine. Increased synthesis of prostaglandins in response to pancreatic secretagogues does not appear to be involved in the process of enzyme secretion.