Nifedipine and alpha adrenoceptors in rat aorta. I. Role of extracellular calcium in alpha-1 and alpha-2 adrenoceptor-mediated contraction.

The ability of nifedipine to inhibit contractions induced by non-selective and selective alpha adrenoceptor agonists and by KCl depolarization was studied in the rat aorta. The presence of alpha-2 adrenoceptors which mediate vasoconstriction was demonstrated. Furthermore, this response was highly dependent on extracellular calcium. Alpha-1 adrenoceptors were also present, but this response was dependent primarily upon intracellular calcium 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 calcium. The fast component was resistant to nifedipine treatment and is therefore assumed to be due to release of intracellular calcium. 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 calcium influx pathways activated by these two types of stimuli 1) may be the same or 2) they have similar affinities for nifedipine or 3) there is a common site of action of nifedipine on both calcium entry pathways.