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

Cholinergic stimulation of vascular prostacyclin synthesis

“…Tho suppression of the cholinergic stimulation aftor mechanical dc'-oridolhoVidI izdLion suggests that this stimulation takes place in the endothelial cells. Ca*''^ scems to play a rôle in the cholinergic action ; this is consistent with our previous observations that carbamylcholino stimulâtes prostaglandin synthesis in the dog thyroid (7) and the rat pancréas (8), by a calcium-dependent mechanism. Although both effects involvo the endothelium, stimulation of 6-K-PGFia production requires higher concentrations of acetylcholine than vascular smooth muscle relaxation: 1 to 10 ;JM versus 0.01 to I ;JM (2,3).…”

The role of phosphoinositiees in signal transduction

“…Not surprisingly, increased arachidonate release is reflected in increased prostaglandin synthesis in several tissues which show a phosphoinositide effect [19,20,67,96,185,304]. However, in the exocrine pancreas the elevation in PI-derived arachidonate on stimulation of enzyme secretion with several agonists is several orders of magnitude higher than the stimulated formation of PGE2 and PGF2~ [19,20,67]. A similar relationship, although less striking, was noted on stimulation of perfused heart or kidney with bradykinin [151].…”

Inhibitory effects of arachidonic acid on muscarinic current response in single pancreatic acinar cells of rats.

“…Pancreatic secretion depends on an increase in [Ca2+]i due to mobilization from internal storage sites by 1P3 (Streb et al 1983(Streb et al , 1985Schulz, 1989). Several studies have demonstrated that AA metabolites (prostaglandins) or inhibitors of AA oxidation (cycloand lipoxygenase pathways) induce no effect on secretagogueinduced amylase release (Chauvelot et al 1979;Bauduin et al 1981;Rubin et al 1982;Stenson & Lobos, 1982). These observations suggest that AA metabolites (prostaglandins and leukotrienes) are not involved in the Ca2+-mobilizing mechanism of receptor stimulation (IP3-induced Ca2+-mobilization mechanism).…”

“…The released AA can be metabolized via both cycloand lipoxygenase pathways, resulting in the formation of prostaglandins and leukotrienes (Rubin, Kelly, Halenda & Laychock, 1982). However, these products of oxidation do not seem to be obligatory intermediates in Ca+-dependent pancreatic protein secretion since secretion evoked by cholinergic and peptidergic stimulation was unaffected by two respective inhibitors of the cyclo-and lipoxygenase metabolic pathways, indomethacin and nordihydroguaiaretic acid (Chauvelot, Heisler, Hout & Gagnon, 1979;Bauduin, Galand & Boeynaems, 1981; Stenson & Lobos, 1982;Rubin et al 1982). Arachidonic MS 8394 acid itself has been shown to affect cell signalling elements in many other cells.…”