Methoctramine tetrahydrochloride is a potent and cardioselective antagonist of the M2 muscarinic receptor, capable of inhibiting muscarine-induced bradycardia in vivo.

Methoctramine tetrahydrochloride effectively inhibits the increase in PG synthesis triggered by Acetylcholine (ACh) and Arecaidine propargyl ester (APE) in a dose-dependent manner[1]. At concentrations ranging from 0.01 to 1 μM, it enhances the contractions resulting from both pre- and postganglionic nerve stimulations in guinea-pig tracheal tubes that are isolated and innervated[2]. Moreover, when the concentration of Methoctramine tetrahydrochloride reaches or exceeds 10 μM, it diminishes the reactions to nerve stimulation as well as to exogenously applied ACh[2].

Methoctramine (300 μg/kg; i.v.) tetrahydrochloride strongly inhibits the Methacholine- and Muscarine-induced bradycardia in the anaesthetized rat, respectively[3].