Regulation by diacylglycerol of calcium-evoked amylase secretion from intact and permeabilized pancreatic acinar cells.
The role of diacylglycerol in the mechanism of amylase release was investigated in isolated rat pancreatic acinar cells. Carbachol produced a time-dependent and dose-related increase in diacylglycerol production which paralleled the time course of amylase secretion. The addition of atropine to acinar cells pretreated with 100 microM carbachol produced a lag in the fall in diacylglycerol levels, which was preceded by a prompt fall in cytosolic Ca2+ and amylase secretion. A threshold concentration of ionomycin amplified the modest action of dioctanoylglycerol on amylase secretion. Ca2(+)-evoked amylase release elicited by saponin permeabilized acinar cells was markedly enhanced by dioctanoylglycerol. These collective findings support the hypothesis that diacylglycerol alone is not an adequate messenger to mediate pancreatic amylase release, but does serve to modulate the actions of Ca2+.
Komabayashi
T
T
Department of Pharmacology, Medical College of Virginia, Richmond.
McKinney
J S
JS
Rubin
R P
RP
D000681:Amylases / Q000378:metabolism*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D002217:Carbachol / Q000494:pharmacology; D002463:Cell Membrane Permeability; D004075:Diglycerides / Q000096:biosynthesis / Q000502:physiology*; D015759:Ionomycin / Q000494:pharmacology; D010179:Pancreas / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D015398:Signal Transduction / Q000187:drug effects*
D004075:Diglycerides; D015759:Ionomycin; D001285:Atropine; D002217:Carbachol; D000681:Amylases; D002118:Calcium