Muscarinic cholinergic stimulation of phosphatidylinositol turnover in the longitudinal smooth muscle of guinea-pig ileum

Abstract

The metabolism of phosphatidylinositol and phosphatidate was investigated in fragments of longitudinal smooth muscle from guinea-pig ileum incubated with cholinergic and anticholinergic drugs. Incorporation of Pi into these lipids was enhanced by acetylcholine and carbamoylcholine. The receptor responsible for triggering this response was of the muscarinic type, since the response was also produced by the muscarinic agonists acetyl-.beta.-methylcholine, carbamoyl-.beta.-methylcholine and pilocarpine, and the response was prevented by atropine and propylbenzilylcholine mustard, but not by tubocurarine. Increased phosphatidylinositol labeling was clearly observed within 5 min in tissue treated with a high concentration of carbamoylcholine. Half-maximal stimulation of phosphatidylinositol labeling occurred at approximately 10.mu.M-carbamoylcholine. Incubation of muscle fragments with carbamoylcholine provoked a decrease in phosphatidylinositol concentration, as would be expected if phosphatidylinositol breakdown is the reaction controlled by agonists. Phosphatidylinositol breakdown may be a reaction intrinsic to the mechanisms of muscarinic cholinergic receptor systems.