José M. Calleja

Comparison of the effects of hydralazine and nifedipine on contractions and 45Ca influx of rat aorta

Abstract— The effect of the vasodilator hydralazine has been compared with nifedipine on KCl‐(K+) (60 mM) and noradrenaline‐(NA) (10 μM) induced 45Ca uptake and contractile responses in rat aorta arterial strips without endothelium. Hydralazine (0.5–10 mM) was equally effective in relaxing K+ ‐ (IC50 = 2.2 ± 0.17 mM) and NA‐(IC50 = 3.06 ± 0.25 mM) induced tension, the degree of relaxation depending on the dose. Nifedipine totally inhibited K+‐(IC50 = 3.16 ± 0.28 nM) induced contractions with lower doses than were necessary to relax (up to 54.0 ± 4.1% with supramaximal concentrations) NA‐induced contractions (IC50 = 1.48 ± 0.12 μM). In the experiments in a calcium‐free medium, nifedipine (1 μM) had no effect on the NA‐(10 μM) induced contractions whereas hydralazine (1 mM) strongly inhibited them. Nifedipine did not affect the basal uptake of 45Ca but the induced uptakes were reduced to 66.3 ± 3.2% (K+) and 65.5 ± 4.1% (NA) of their basal values. Hydralazine did not affect the basal uptake of 45Ca nor that induced by the two vascoconstrictor agents. These results suggest that nifedipine acts on the cell membrane by blocking the movements of calcium through the voltage‐dependent and receptor‐operated calcium channels, whilst hydralazine has an intracellular effect.

Study of the in vivo and in vitro cardiovascular effects of (+)-glaucine and N-carbethoxysecoglaucine in rats.

1 The cardiovascular and vasorelaxant effects of (+)‐glaucine and of a semisynthetic derivative (N‐carbethoxysecoglaucine) were studied in rats.