Effects of prostaglandin of E, F and I series, leukotriene C and platelet activating factor on amylase release from isolated rat pancreatic acini.
Exogenous eicosanoids were reported to affect pancreatic secretion, but it is unknown whether this effects is mediated by the changes in pancreatic circulation or by direct action on pancreatic secretory cells. In this study the effects of prostaglandins (PG), leukotriene C4 (LTC4) and platelet activating factor (PAF) and the blockers of their biosynthesis or receptor antagonists on amylase release from the isolated rat pancreatic acini were examined. The acini were incubated with pancreatic secretagogues, such as caerulein or urecholine in the presence or absence of various concentrations (10(-9)-10(-5) M) of PGE2, Nocloprost (stable analog of PGE2), PGI2, PGF1 alpha, LTC4, PAF, indomethacin (inhibitor of endogenous PG formation) and A-63162 (blocker of endogenous LT biosynthesis). PGE2, PGI2 and PGF1 alpha inhibited secretagogues-stimulated enzyme secretion from isolated pancreatic acini but their inhibitory potency was about 1000 times lower, on molar basis, than that of Nocloprost. PAF and LTC4 produced concentration-dependent stimulation of amylase release from the unstimulated acini reaching about 50% of caerulein-induced maximal response and enhanced amylase release induced by caerulein or urecholine. The effects of PAF and LTC4 were reversed by the addition of respective receptor antagonist for PAF (TCV-309) and for LTC4 (FPL-55712). These results indicate that PG inhibit, while PAF and LTC4 stimulate pancreatic enzyme secretion and thus could be implicated in the control of this secretion.
Jaworek
J
J
Institute of Physiology, University School of Medicine, Cracow, Poland.
Konturek
S J
SJ
D000081:Acetamides / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D001626:Bethanechol Compounds / Q000494:pharmacology; D002108:Ceruletide / Q000494:pharmacology; D002867:Chromones / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D017997:Leukotriene C4 / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D008297:Male; D010179:Pancreas / Q000033:anatomy & histology / Q000187:drug effects / Q000201:enzymology*; D010647:Phenyl Ethers; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011448:Prostaglandin Antagonists; D011453:Prostaglandins / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology; D011726:Pyridinium Compounds / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D044005:Tetrahydroisoquinolines
D000081:Acetamides; D001626:Bethanechol Compounds; D002867:Chromones; D007546:Isoquinolines; D010647:Phenyl Ethers; D010972:Platelet Activating Factor; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011460:Prostaglandins F; D011461:Prostaglandins F, Synthetic; D011726:Pyridinium Compounds; D044005:Tetrahydroisoquinolines; C068663:N-hydroxy-N-(1-(4-(phenylmethoxy)phenyl)ethyl)-acetamide; D017997:Leukotriene C4; C048895:nocloprost; D002108:Ceruletide; C006312:FPL 55712; D011464:Epoprostenol; D000681:Amylases; D015232:Dinoprostone; C067430:TCV 309; C100006:prostaglandin F1; D007213:Indomethacin