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PMID: 3010833 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S. Review

Identification of cellular activation mechanisms associated with salivary secretion.

Annual review of physiology ·Vol. 48 ·1986-00-00 ·Pages 75-88

Putney JW

Abstract

In recent years, our understanding of receptor-signalling mechanisms in the salivary glands has advanced considerably. Two receptor pathways exist, one involving cAMP, which primarily regulates enzyme secretion, and another involving the hydrolysis of PIP2, which regulates Ca2+ mobilization and, subsequently, monovalent ion fluxes probably important in ion and water secretion in the intact gland. Mobilization of Ca2+ results from both the release of internal Ca2+, and from Ca2+ entry from the extracellular space. The signal for Ca2+ release appears to be (1,4,5)IP3, one of the water soluble products of PIP2 hydrolysis. The mechanism controlling Ca entry is not understood, but speculation abounds. Hydrolysis of PIP2 also produces DG, which has a messenger role in activating a specific protein kinase, the C kinase. The C kinase interacts with Ca2+ mobilization in some as yet uncharacterized way in regulating enzyme secretion.

MeSH Terms
Adenosine Triphosphate/metabolism Animals Calcium/metabolism Cell Membrane Permeability Cyclic AMP/metabolism In Vitro Techniques Inositol/metabolism Lipid Metabolism Mice Parotid Gland/metabolism Phosphatidylinositols/metabolism Potassium/metabolism Protein Kinase C/metabolism Rats Receptors, Adrenergic/physiology Receptors, Cholinergic/physiology Rubidium/metabolism Saliva/metabolism Salivary Glands/metabolism
Chemicals
Phosphatidylinositols Receptors, Adrenergic Receptors, Cholinergic Inositol Adenosine Triphosphate Cyclic AMP Protein Kinase C Rubidium Potassium Calcium
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Putney J W
Article Info
Journal
Annual review of physiology
Abbr.
Annu Rev Physiol
ISSN
0066-4278
Published
1986-00-00
Pages
75-88
Language
English
Region
United States
NLM ID
0370600
Subset
IM
Grants
NIDCR NIH HHS · DE-05764 · United States
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