Inositol trisphosphate independent increase of intracellular free calcium and amylase secretion in pancreatic acini

Ashok Saluja, Robert E. Powers, Michael L. Steer

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

It is generally believed that the activation of various cell surface receptors results in the phospholipase C-catalyzed production of inositol trisphosphate which, in turn, increases the intracellular concentration of free Ca2+ by stimulating its release from non-mitochondrial sources. We have investigated both the production of inositol trisphosphate and changes in intracellular Ca2+ concentration in rat pancreatic acini in response to caerulein and CCK-JMV-180, two analogs of cholecystokinin. Both of these analogs cause comparable increases in the rate of amylase secretion and in intracellular Ca2+ concentration but their effects on inositol phosphate generation are dramatically different; caerulein stimulates significant production of inositol phosphates within 1 min of its addition, whereas no detectable levels of inositol phosphates were generated within the same time after addition of CCK-JMV-180. These results suggest that the CCK-JMV-180 stimulated release of intracellular Ca2+ is not mediated by inositol trisphosphate but some other as yet unidentified messenger.

Original languageEnglish (US)
Pages (from-to)8-13
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume164
Issue number1
DOIs
StatePublished - Oct 16 1989
Externally publishedYes

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Inositol Phosphates
Inositol
Amylases
Ceruletide
Calcium
Cholecystokinin
Cell Surface Receptors
Type C Phospholipases
Rats
Chemical activation
JMV 180

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Inositol trisphosphate independent increase of intracellular free calcium and amylase secretion in pancreatic acini. / Saluja, Ashok; Powers, Robert E.; Steer, Michael L.

In: Biochemical and Biophysical Research Communications, Vol. 164, No. 1, 16.10.1989, p. 8-13.

Research output: Contribution to journalArticle

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