Lee Kwang Kook, Uhm Dae-Yong, Park Myoung Kyu
Department of Physiology, Sungkyunkwan University School of Medicine, 300 Chunchundong, Janganku, Suwon 440-746, South Korea.
FEBS Lett. 2003 Mar 13;538(1-3):134-8. doi: 10.1016/s0014-5793(03)00165-0.
We have investigated whether low affinity cholecystokinin (CCK) receptors suppress agonist-induced rises of cytosolic free Ca(2+) concentration ([Ca(2+)]c) in pancreatic acinar cells by using properties of caffeine. A high concentration of caffeine (20 mM) completely blocked inositol 1,4,5-trisphosphate (InsP(3))-induced [Ca(2+)]c rises but spared the InsP(3)-independent long-lasting [Ca(2+)]c oscillations. In the presence of 20 mM caffeine, only high concentrations of CCK, but not bombesin or JMV-180, suppressed the caffeine-resistant CCK or bombesin-induced [Ca(2+)]c oscillations, indicating that low affinity CCK receptors inhibit agonist-induced [Ca(2+)]c oscillations. It could be one of the underlying mechanisms by which low affinity CCK receptors suppress secretion in pancreatic acinar cells.