title: Is thioridazine-induced ejaculation failure peripheral in origin?
abstract: The contractile response of rabbit vas deferens to the field stimulation was almost equally depressed by thioridazine and chlorpromazine. Phenoxybenzamine in a dose of 10(-7) g/ml augmented the response slightly, while in a dose of 10(-6) g/ml slightly depressed. The contractile response to exogenously administered noradrenaline was remarkably depressed by thioridazine and chlorpromazine and completely abolished by phenoxybenzamine. Almost equal potencies of sympatholytic effects of thioridazine and chlorpromazine may exclude the possibility that thioridazine-induced ejaculation failure, which is higher incidence than the failure induced by chlorpromazine, is due to its inhibitory action on peripheral adrenergic mechanism.
mesh_terms: D000818:Animals; D002746:Chlorpromazine / Q000494:pharmacology; D003864:Depression, Chemical; D004542:Ejaculation / Q000187:drug effects*; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D010643:Phenoxybenzamine / Q000494:pharmacology; D011817:Rabbits; D013881:Thioridazine / Q000494:pharmacology*; D014649:Vas Deferens / Q000187:drug effects*
chemical_list: D010643:Phenoxybenzamine; D013881:Thioridazine; D002746:Chlorpromazine; D009638:Norepinephrine