Methoctramine tetrahydrochloride

Methoctramine tetrahydrochloride is a potent and cardioselectivity antagonist of M2 muscarinic receptor. Methoctramine tetrahydrochloride can inhibit Muscarine-induced bradycardia in vivo[1][2][3].

Signaling Pathways >> Neuronal Signaling >> mAChR

Research Areas >> Cardiovascular Disease

Signaling Pathways >> GPCR/G Protein >> mAChR

M2 muscarinic receptor[1]

Methoctramine tetrahydrochloride attenuates Acetylcholine (ACh)- and Arecaidine propargyl ester (APE)-induced increases in PG synthesis in a concentration-dependent manner[1]. Methoctramine (0.01-1 μM) tetrahydrochloride causes facilitation of contractions induced by both pre- and postganglionic nerve stimulation in the guinea-pig isolated, innervated tracheal tube preparation[2]. Methoctramine (≥10 μM) tetrahydrochloride reduces responses to both nerve stimulation and exogenous ACh[2].

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

[1]. Jaiswal N, et, al. Methoctramine, a cardioselective antagonist: muscarinic receptor mediating prostaglandin synthesis in isolated rabbit heart. Eur J Pharmacol. 1991 Jan 3;192(1):63-70.

[2]. Watson N, et, al. Actions of methoctramine, a muscarinic M2 receptor antagonist, on muscarinic and nicotinic cholinoceptors in guinea-pig airways in vivo and in vitro. Br J Pharmacol. 1992 Jan;105(1):107-12.

[3]. Wess J, et, al. Methoctramine selectively blocks cardiac muscarinic M2 receptors in vivo. Naunyn Schmiedebergs Arch Pharmacol. 1988 Sep;338(3):246-9.