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European Heart Journal 1985 6(9):730-736;
Copyright © 1985 by the European Society of Cardiology.
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© 1985 The European Society of Cardiology

Chronotropic action of alinidine on the isolated sinus node of the rabbit heart

R. HABERL and G. STEINBECK

Medizinische Klinik I der Universität München, Klinikwn Großhadern, Marchionistraße 15 D8000 München, F.R.G.

Received 12 December 1984; .

Abstract

The main action of alinidine, proposed for the treatment of angina pectoris, is a reduction of heart rate. To evaluate this negative chronotropic action, we studied the effect of the drug (concentrations ranging from 0.57 to 29 x 10°M) on sinus rate and pacemaker location by multiple intracellular impalements in 31 isolated rabbit right atria. Alinidine caused a dose-dependent prolongation of the spontaneous cycle length which amounted to 58 ms±28 (13%± 7) (±1 SD) compared with control at 2.9 µM. Corrected sinus node recovery time increased from 83 ms ±47 to 126 ms ±80. Higher concentrations did not further increase the cycle length. The bradycardiac action was due to a selective slowing of phase 4-depolarization of pacemaker fibres. Amplitude and duration of the transmembr one potential of dominant fibres remained unchanged. However, repolarization of latent and atrial fibres was prolonged. A trial effective refractory period increased by about 10%. The electrophysiologic effects of clonidine in equimolar concentrations were similar to alinidine. This study identifies slowing of phase 4-depolarization of dominant fibres as cause of the negative chronotropic action of alinidine. Pacemaker location and sinoatrial conduction time were unaffected.

Key Words: Slowing of phase 4 depolarization • sinoatrial conduction


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