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Studies on the characterization of the subtype(s) of muscarinic receptor involved in prostacyclin synthesis in rabbit cardiomyocytes.

The present study was conducted to localize and characterize the subtype(s) of muscarinic receptor involved in prostacyclin (PGI2) production elicited by the cholinergic transmitter acetylcholine (ACh) in various cell types in the rabbit heart. ACh increased PGI2 synthesis measured as 6-keto-PGF1 alpha, in cultured coronary endothelial cells and freshly dissociated ventricular myocytes in a dose dependent manner but not in cultured coronary smooth muscle cells of rabbit heart. McN-A-343, a partially selective M1 muscarinic ACh receptor (mAChR) agonist, did not alter 6-keto-PGF1 alpha synthesis in these cell types. ACh induced 6-keto-PGF1 alpha synthesis in coronary endothelial cells and ventricular myocytes was not altered by a low concentration (10(-8) M) of pirenzipine, an M1 mAChR antagonist but was reduced by a higher concentration (10(-6) M). In coronary endothelial cells ACh induced 6-keto-PGF1 alpha production was reduced by hexahydro-sila-difendial (HHSiD), an M3 mAChR antagonist, and in ventricular myocytes by both 11-¿2-[(di-ethylamino) methyl]-1-piperidinyl]acetyl-5,11-dihydro-6-H-pyrido-[2,3-b]-benzodiazep ine-6 one¿ (AF-DX 116), an M2 receptor antagonist, and HHSiD. The decrease by ACh of isoporterenol stimulated cAMP accumulation was minimized by AF-DX 116 but not by HHSiD or pirenzipine. Pertussis toxin treatment minimized ACh induced decrease in isoproterenol stimulated rise in cAMP and ATP release, but not ACh induced 6-keto-PGF1 alpha synthesis. These data suggest that ACh stimulates prostacyclin production in coronary endothelial cells via M3 mAChR and in ventricular myocytes M2 and M3 mAChR. Moreover, ACh induced decrease in cAMP, but not the increase in 6-keto-PGF1 alpha production, is mediated by pertussis toxin sensitive G alpha i proteins in these cells.