On the Mechanism Involved in the Ability of Meptazinol to Potentiate the Effects of Sympathetic Nerve Stimulation

Abstract

Abstract Mouse isolated vas deferens responded to field stimulation (0.1 Hz) with twitch responses which were abolished by ag-methyleneadenosine 5′-triphosphate (0.5 p μM) and were potentiated 2 to 3 fold by meptazinol(5–300 p μM). Exogenous adenosine 5′-triphosphate (4–30 p μM) also caused a twitch response but was unaffected by meptazinol(30 p μM) as was the response to phenylephrine. The effect of meptazinol on the electrically-induced twitch was reproducible, fast in onset, easily reversed by washing and was still seen in the presence of prazosin (1 p μM), yohimbine (1 p μM), propranolol(O.1 p μM), atropine (0.1 p μM), physostigmine (1 p μM), cocaine (1 p μM) or desmethylimipramine (0.3 p μM) indicating that the mechanism involved does not depend on adrenoceptors, cholinergic mechanisms or blockade of uptake,. Mouse isolated atria responded to stimulation (1, 2 or 5 Hz) of their sympathetic nerves via transmural electrodes with chronotropic responses which were abolished by atenolol(5 and 50 p μM) but were unaffected by ag-methyleneadenosine 5′-triphosphate (0.5 p μM). Meptazinol (100 p μM) failed to potentiate the responses. It is suggested that meptazinol potentiates the effects of the non-adrenergic non-cholinergic transmitter thought to be involved in the response of the mouse vas deferens to electrical stimulation.