Cellular mechanisms mediating agonist-stimulated calcium influx in the pancreatic acinar cell.

Journal Article (Journal Article;Review)

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.

Full Text

Duke Authors

Cited Authors

  • Pandol, SJ; Gukovskaya, A; Bahnson, TD; Dionne, VE

Published Date

  • March 23, 1994

Published In

Volume / Issue

  • 713 /

Start / End Page

  • 41 - 48

PubMed ID

  • 8185204

International Standard Serial Number (ISSN)

  • 0077-8923

Digital Object Identifier (DOI)

  • 10.1111/j.1749-6632.1994.tb44051.x


  • eng

Conference Location

  • United States