The Effect of Nifedipine on Isolated Human Peripheral Vessels

Isometric tension was recorded in ring preparations of human peripherial arteries and veins contracted by potassium (127mM) and noradrenaline (1.8 X 10(-5)M). In the veins, nifedipine had a marked relaxing effect on contractions induced by both agents, and also reduced the contractile amplitude when added prior to stimulation. The inhibiting effect of nifedipine was more marked on the potassium than on the noradrenaline-evoked responses. This was in contrast to verapamil, which inhibited the noradrenaline-induced contractions significantly more, than those produced by potassium. After immersion of the vein preparations in calcium-free medium for 30 min., the potassium contracture decreased to 26+/2.0% (mean +/ S.E.M.) of the response in normal Krebs solution, and the noradrenaline-evoked to 7.1+/0.8%. The responses to both agents were completely restored when the calcium concentration was increased from 0 to 4 mM. Nifedipine (1.5X10(-7)M) depressed the potassium contracture in calcium-free solution to 7.3+/1.6%, and the noradrenaline response to 5.5+/1.6%; on addition of calcium, the response elicited by potassium increased to 16+/1.7%, and that by noradrenaline to 56+/8.6%. Compared with its actions on the veins, the effect of nifedipine on the arterial preparations was less pronounced. In the arteries, too, the inhibiting effect of nifedipine was significantly more pronounced on the potassium than on the noradrenaline-induced contraction. Immersion for 30 min. in calcium-free medium reduced the response to potassium to 61+/6.0% and that to noradrenaline to 68+/5.6% of the control in normal Krebs. Nifedipine (2.9X10(-7)M) further reduced the potassium contraction to 20+/4.0%; the response to noradrenaline was unaffected, being 74+/6.4% of the control.