Evidence for the convergence of β-adrenergic and muscarinic signalling systems at a post-receptor site

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.