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The effects of drugs inhibiting catecholamine uptake on tyramine and noradrenaline‐induced contractions of the isolated rat vas deferens
Author(s) -
BARNETT A.,
SYMCHOWICZ S.,
TABER R. I.
Publication year - 1968
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1968.tb08476.x
Subject(s) - tyramine , vas deferens , imipramine , long term potentiation , endocrinology , medicine , chemistry , catecholamine , adrenergic , pharmacology , norepinephrine , biology , dopamine , receptor , alternative medicine , pathology
1 . Cocaine did not antagonize the tyramine‐induced contractile response of the isolated rat vas deferens at the same concentrations which markedly potentiated the contractile response to noradrenaline. 2 . Imipramine and amitriptyline non‐competitively antagonized the contractile response to tyramine but did not potentiate noradrenaline. Desmethylimipramine produced both potentiation of noradrenaline and antagonism of tyramine. 3 . Dexchlorpheniramine non‐competitively antagonized the contractile response to tyramine. It also produced an atypical potentiation of noradrenaline in which lower concentrations of noradrenaline were potentiated to a greater extent than higher ones. 4 . Imipramine inhibited the in vitro uptake of noradrenaline‐ 3 H in rat vas deferens as did cocaine, desmethylimipramine and dexchlorpheniramine. These results suggest that the α‐adrenergic blocking property of imipramine masks the potentiation of noradrenaline by uptake inhibition. 5 . Evidence is also presented which suggests that α‐adrenergic blockade of released noradrenaline may be the major mechanism for tyramine inhibition by imipramine‐like drugs. This may explain why cocaine, which has no real alpha blocking action, is ineffective against tyramine.