• 1 January 1978
    • journal article
    • research article
    • Vol. 204  (1) , 175-182
Abstract
The effects of 2,4,6-triaminopyrimidine (TAP) were studied in vitro on transmembrane potential and contractility in guinea-pig myocardium. In electrically driven Langendorff-perfused hearts, the addition of 1 and 5 mM TAP produced an initial dose-dependent positive inotropic response with no change in resting tension. The activation process was studied by means of microelectrode and tension recording from isolated electrically driven guinea-pig left atrial preparations. TAP (1-10 mM) produced dose-dependent changes in both electrical and mechanical properties of the tissue. In particular, 1, 5 and 10 mM TAP increased the action potential duration by approximately 20, 40 and 60% while also increasing contractile strength by approximately 30, 60 and 90%, resectively. The mechanical effects of TAP were also observed in the presence of 10 .mu.M propranolol. Experiments on catecholamine-restored hearts which were depolarized by K indicated that the inotropic action of TAP was associated with slow Ca influx channels. The inotropic effects of TAP were reduced by D600 [.alpha.-isopropyl-.alpha.-[(N-methyl-N-homoveratryl)-V-aminopropyl]-3,4,5-trimethoxyphenylacetonitrile hydrochloride], a Ca antagonistic agent. The inotropic actions of TAP probably result from a decrease in K conductance as a result of the inhibition of Ca++-K+ interactions at the inner surface of the myocardial membrane.

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