Lee_1989_Eur.J.Pharmacol_167_295

The cardioselective muscarinic antagonist methoctramine antagonized carbamylcholine-mediated phosphoinositide (PI) hydrolysis in a concentration-dependent fashion in dissociated rat cerebrocortical cells. However, as the concentration of methoctramine was increased above 5 microM, there was a reversal of the antagonism of the PI response. In the absence of carbamylcholine, methoctramine by itself significantly increased PI hydrolysis with a maximal effect at 30 microM. Various classes of receptor antagonists, including atropine, and ion-channel blockers were unable to block methoctramine-stimulated PI hydrolysis.