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Evidence for the convergence of β‐adrenergic and muscarinic signalling systems at a post‐receptor site
Author(s) -
Horn Valerie J.,
Baum Bruce J.,
Ambudkar Indu S.
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)81604-7
Subject(s) - muscarinic acetylcholine receptor , endocrinology , medicine , chemistry , stimulation , phosphatidylinositol , muscarinic antagonist , atropine , agonist , receptor , biology , signal transduction , biochemistry
The β‐adrenergic agonist isoproterenol stimulates inositol trisphosphate (IP 3 ) formation and cytosolic Ca 2+ ([Ca 2+ ] i ) mobilization in rat parotid acini via a cAMP‐dependent process. Atropine, a muscarinic antagonist, inhibited these isoproterenol responses without affecting isoproterenol‐induced amylase secretion or peak [Ca 2+ ] i and IP 3 responses elicited by α 1 ‐adrenergic stimulation with epinephrine. Atropine had no effect on isoproterenol‐induced [Ca 2+ ] i responses in a cell line which lacked muscarinic receptors and did not alter β‐adrenoreceptor ligand binding. These results suggest that the inhibition by atropine results from a post‐receptor effect on cAMP‐mediated stimulation of phosphatidylinositol 4,5 bisphosphate (PIP 2 ) hydrolysis.