• 1 January 1983
    • journal article
    • research article
    • Vol. 224  (2) , 443-450
Abstract
Experiments were performed on isolated rat aorta and superior mesenteric artery in order to study the action of nifedipine on norepinephrine and K-depolarization-evoked contractions, and transmembrane Ca fluxes. Concentration-dependent contractions were obtained with norepinephrine in physiological solution and with Ca2+ in K-depolarizing solution. Nifedipine caused a concentration-dependent depression of the maximum response. When aorta was depolarized by 40 mM KCl (instead of usual 100 mM KCl concentration), high concentrations of Ca2+ evoked a relaxation that was also blocked by nifedipine. The action of nifedipine was examined on Ca influx and efflux in arteries stimulated by norepinephrine and K-depolarization. Norepinephrine-evoked Ca influx, but not Ca efflux, was reduced by nifedipine. Concentration inhibitory curves for Ca influx and contraction could be superimposed. K-depolarization-dependent Ca entry and Ca efflux were blocked by nifedipine at concentrations lower than those required to antagonize norepinephrine actions. The action of nifedipine on artery contractility can apparently be related to blockade of Ca entry through channels opened during depolarization or receptor-response coupling.