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- W1967939449 abstract "Triamterene (TA) inhibits in the μm range, as was previously shown in our laboratory, the positive inotropic action of beta-adrenoceptor agonists like isoproterenol in atrial preparations, when applied first. This interaction may be best explained by a direct influence of TA on the beta-adrenergic receptor-site itself or by an uncoupling of the signal transfer between receptor and adenylate cyclase complex at the inner sarcolemmal membrane site. For clarification we performed biochemical studies at freshly prepared membrane particles from guinea-pig hearts, combining both hypothetical sites of interaction. Binding studies with [3H]-dihydroalprenolol to the myocardial beta-adrenoceptor revealed that TA (1 to 10 μmol/l) did not disturb their functioning excluding a possible interaction at this membrane site. On the other hand we found a non competitive inhibition of the isoprenaline-activated adenylate cyclase while basic activity was not altered in the presence of triamterene (TA, 5 to 200 μmol/l). From the concentration-response curves a Ki-value of TA for half-maximal inhibition of 2.8 μmol/l was calculated. Since the sodium fluoride activated adenylate cyclase was also inhibited by triamterene in the same concentration range we conclude that it interferes with the signal-transfer between the beta-adrenoceptor site and the adenylate cyclase system through the plasmalemma." @default.
- W1967939449 created "2016-06-24" @default.
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- W1967939449 date "1983-05-01" @default.
- W1967939449 modified "2023-09-26" @default.
- W1967939449 title "The interaction of triamterene at the myocardial beta receptor site" @default.
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- W1967939449 doi "https://doi.org/10.1016/0022-2828(83)91343-3" @default.
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