Cellular mechanisms and physiological implications of quantal Ca2+ release in pancreatic acinar cells.
Previous studies in pancreatic acini demonstrated that submaximal concentrations of agonist release only a portion of Ca2+ from the intracellular pool during the first few seconds of stimulation. Despite continued stimulation, no further release of pool Ca2+ takes place. This process has been termed quantal release. Previous hypotheses have proposed that quantal release results from varying sensitivities of the intracellular pool to inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ release. The purpose of the present experiments was to further characterize the cellular mechanism of quantal release and to determine the role of quantal release in pancreatic enzyme secretion. The results indicate that the phenomenon of quantal calcium release is not due to varying sensitivities of the intracellular Ca2+ stores to IP3. Quantal release results from both an intrinsic property of the IP3 receptor, which causes it to transport Ca2+ transiently, and from the transient nature of the increase in IP3 generated by submaximal agonist concentration. With this mechanism, sequential additions of physiological concentrations of agonist cause transient increases in intracellular Ca2+ concentration leading to bursts of enzyme secretion.
Rutherford
R E
RE
Department of Medicine, Department of Veterans Affairs Medical Center, San Diego, California.
Schoeffield-Payne
M
M
Pandol
S J
SJ
D000681:Amylases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D002766:Cholecystokinin / Q000494:pharmacology; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D010179:Pancreas / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D015544:Inositol 1,4,5-Trisphosphate; D002217:Carbachol; D002766:Cholecystokinin; D000681:Amylases; D002118:Calcium