ACTION-POTENTIAL, MEMBRANE CURRENTS AND FORCE OF CONTRACTION IN MAMMALIAN HEART-MUSCLE FIBERS TREATED WITH QUINIDINE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 216  (1) , 176-182
Abstract
The effects of quinidine on electrical and mechanical activity were investigated in atrial and/or ventricular heart muscle preparations from guinea pigs and cats. Quinidine (1-100 .mu.M) exerted negative inotropic effects in papillary muscles from guinea pigs and cats. In guinea pig left atria, a positive inotropic effect was superimposed on the negative inotropic effect in response to quinidine. Quinidine (100 .mu.M) prolonged the duration of the action potential in guinea pig atria but shortened it in guinea pig ventricular muscle. In cat papillary muscles, the late repolarization phase was markedly prolonged by quinidine, but virtually no change of the plateau phase was observed. The maximal rate of rise and the resting potential were reduced by quinidine in all preparations. Voltage clamp experiments in cat ventricular muscle revealed that the Ca-dependent slow inward current and the outward current of K were decreased by quinidine. The effects of quinidine on slow inward current and force of contraction in ventricular muscle were antagonized by isoprenaline (1 .mu.M). The effects of quinidine and the different changes of the action potential configuration can be explained by an unspecific inhibition of the currents of Na, Ca and K. The negative inotropic effect of quinidine is probably related to the depressing effect of the drug on the Ca-dependent slow inward current. The positive inotropic effect of the drug in atrial heart muscle could be related to the prolongation of the action potential which may indirectly improve the influx of Ca during excitation.

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