PMID: 375748May 1, 1979Paper

Calcium mediation of cholinergic-stimulated amylase release from mouse parotid gland

The American Journal of Physiology
E L WatsonI A Siegel

Abstract

Amylase release from mouse parotid fragments was stimulated independently by cholinergic and beta-adrenergic agents. The cholinergic agonist, carbachol, significantly increased release of amylase only in Ca2+ containing medium whereas isoproterenol-stimulated amylase release was unaffected by Ca2+ removal. The ionophore, A23187, mimicked the effect of cholinergic stimulation when Ca2+ was present in the medium. Uptake of 45Ca2+ into tissue fragments was enhanced by carbachol and A23187 but not by isoproterenol; atropine blocked the effect of carbachol. Diphenylhydantoin (DPH) and verapamil partially inhibited carbachol-stimulated amylase release and 45Ca2+ uptake, whereas diazoxide potentiated these effects; in all cases there was good parallelism between 45Ca2+ uptake and amylase release. It was concluded that the primary step in the release of amylase from mouse parotid gland in response to cholinergic agents is an increased influx of Ca2+.

References

Jul 29, 1977·Pflügers Archiv : European journal of physiology·H R KoelzI Schulz
Jun 1, 1975·The American Journal of Physiology·J A Williams, D Chandler
Dec 1, 1974·The Journal of Physiology·D E Chandler, J A Williams

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Citations

Jan 1, 1992·Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists·D O QuissellF J Dowd
Feb 1, 1984·Journal of Dental Research·E WatsonH Horwitz
Apr 1, 1980·Pflügers Archiv : European journal of physiology·D Templeton
May 1, 1981·Experimental Lung Research·F Al-Bazzaz, T Jayaram
Nov 8, 1982·Life Sciences·E L WatsonF Dowd
Aug 25, 1986·Life Sciences·E L Watson, K L Jacobson
Feb 28, 1983·Biochemical and Biophysical Research Communications·E L Watson, F J Dowd
May 1, 1980·Kidney International·J A Arruda, S Sabatini

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