Cellular mechanisms mediating agonist-stimulated calcium influx in the pancreatic acinar cell.
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.
Pandol
S J
SJ
Department of Medicine, University of California, San Diego.
Gukovskaya
A
A
Bahnson
T D
TD
Dionne
V E
VE
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
D002766:Cholecystokinin; D006152:Cyclic GMP; D000109:Acetylcholine; D002118:Calcium