Experimental Pharmacological Investigations of Effects of Nifedipine on Atrioventricular Conduction in Comparison with Those of Other Coronary Vasodilators

  • N. Taira
  • S. Motomura
  • A. Narimatsu
  • T. Iijima
Conference paper

Abstract

Pharmacological investigations carried out so far on the cardiovascular actions of nifedipine (Adalat) (VATER et al. [10]; HASHIMOTO et al. [6]) have revealed that nifedipine is the most potent coronary vasodilator ever synthesized. The mechanism of its vasodilator action has been ascribed to the calcium antagonistic action: inhibition of the transmembrane calcium influx of the vascular smooth muscle to reduce the tone (FLECKENSTEIN et al. [3]; GRUN and FLECKENSTEIN [4]). On the other hand, it has been suggested that the ionic channel operative in excitation of cells in the atrioventricular (A-V) junctional area concerned in the major delay of A-V conduction is a slow channel which allows the transmembrane inflow of calcium, sodium ions or both (ZIPES and MENDEZ [12]). A coronary vasodilator, verapamil, the mechanism of action of which has also been described as that of calcium antagonism (GRÜN and FLECKENSTEIN [4]), is able to block this slow channel and cause impairment of A-V conduction (ZIPES and FISCHER [11]). From a therapeutic point of view, however, the impairment of A-V conduction by coronary vasodilators is one of their untoward effects. Thus, it is worthy to examine whether nifedipine as a potent calcium antagonist might impair A-V conduction. The present study was carried out in an attempt to elucidate this point. To characterize the effect of nifedipine on A-V conduction, comparison was made with those of other coronary vasodilators—verapamil, diltiazem (SATO et al [9]), dipyridamole and dilazep. Diltiazem is thought to dilate the coronary vascular bed probably by a calcium antagonistic action (KIYOMOTO, personal communication), whereas dilazep is thought to do so by potentiation of the action of endogenous adenosine (BUYNISKI et al. [2]) like dipyridamole (BRETSCHNEIDER et al. [1]).

Keywords

Manganese Rubber Respiration Adenosine Hydrochloride 

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Copyright information

© Springer-Verlag Berlin Heidelberg 1975

Authors and Affiliations

  • N. Taira
    • 1
  • S. Motomura
    • 1
  • A. Narimatsu
    • 1
  • T. Iijima
    • 1
  1. 1.Department of Pharmacology and Experimental TherapeuticsTohoku University School of MedicineSendaiJapan

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