NIFEDIPINE AND ALPHA ADRENOCEPTORS IN RAT AORTA .1. ROLE OF EXTRACELLULAR CALCIUM IN ALPHA-1 AND ALPHA-2 ADRENOCEPTOR-MEDIATED CONTRACTION

Abstract

The ability of nifedipine to inhibit contractions induced by non-selective and selective .alpha.-adenoceptor agonists and by KCl depolarization was studied in the rat aorta. The presence of .alpha.2-adrenoceptors which mediate vasoconstriction was demonstrated. This response was highly dependent on extracellular Ca. .alpha.1-Adrenoceptors were also present, but this response was dependent primarily on intracellular Ca stores. Contractions induced by maximally effective concentrations of agonists were separated into fast and slow components of the response. Nifedipine effectively inhibited the slow component of contractions induced by norepinephrine, phenylephrine and clonidine. The slow component of the response induced by these agonists is, therefore, due to influx of extracellular Ca. The fast component was resistant to nifedipine treatment and is, therefore, assumed to be due to release of intracellular Ca. Nifedipine was equally potent at inhibiting the slow component of both .alpha.1 and .alpha.2 adrenoceptor-stimulated contractions and contractions due to KCl depolarization. This suggests that the Ca influx pathways activated by these 2 types of stimuli may be the same; they have similar affinities for nifedipine; or there is a common site of action of nifedipine on both Ca entry pathways.