title: Cellular mechanisms mediating agonist-stimulated calcium influx in the pancreatic acinar cell.
abstract: Figure 1 summarizes our current concept of a signaling mechanism to explain agonist-induced Ca2+ entry in the pancreatic acinar cell. We propose that cGMP can modulate Ca2+ entry under conditions of internal Ca2+ store depletion and that the NO signaling system may be involved in coupling Ca2+ depletion to cGMP formation. The finding that Ca2+ entry after Ca2+ store depletion can occur with no elevation in [Ca2+]i37 raises the possibility that alternative signaling pathways may converge to stimulate cGMP formation or that additional messengers may activate plasmalemmal Ca2+ entry mechanisms in parallel.
authors.affiliation: Department of Medicine, University of California, San Diego.
authors.forename: S J
authors.initials: SJ
authors.lastname: Pandol
authors.forename: A
authors.initials: A
authors.lastname: Gukovskaya
authors.forename: T D
authors.initials: TD
authors.lastname: Bahnson
authors.forename: V E
authors.initials: VE
authors.lastname: Dionne
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002766:Cholecystokinin / Q000494:pharmacology* / Q000502:physiology; D006152:Cyclic GMP / Q000502:physiology*; D008954:Models, Biological; D010179:Pancreas / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D015290:Second Messenger Systems; D015398:Signal Transduction
chemical_list: D002766:Cholecystokinin; D006152:Cyclic GMP; D000109:Acetylcholine; D002118:Calcium