The Effect of Nifedipine on Isolated Human Peripheral Vessels

Abstract

Isometric tension was recorded in ring preparations of human peripherial arteries and veins contracted by K (127 mM) and noradrenaline [norepinephrine] 1.8 .times. 10-5 M). In the veins, nifedipine had a marked relaxing effect on contractions induced by both agents and reduced the contractile amplitude when added prior to stimulation. The inhibiting effect of nifedipine was more marked on the K than on the noradrenaline-evoked responses. This was in contrast to verapamil, which inhibited the noradrenaline-induced contractions significantly more, than those produced by K. After immersion of the vein preparations in Ca-free medium for 30 min, the K contracture d-creased to 26 .+-. 2.0% (mean .+-. SEM [standard error of the mean]) of the response in normal Krebs solution, and the noradrenaline-evoked response to 7.1 .+-. 0.8%. The responses to both agents were completely restored when the Ca concentration was increased from 0 to 4 mM. Nifedipine (1.5 .times. 10-7 M) depressed the K contracture in Ca-free solution to 7.3 .+-. 1.6%, and the noradrenaline response to 5.5 .+-. 1.6%; on addition of Ca, the response elicited by K 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, the inhibiting effect of nifedipine was significantly more pronounced on the K than on the noradrenaline-induced contraction. Immersion for 30 min in Ca-free medium reduced the response to K to 61 .+-. 6.0% and that to noradrenaline to 68 .+-. 5.6% of the control in normal Krebs. Nifedipine (2.9 .times. 10-7 M) further reduced the K contraction to 20 .+-. 4.0%; the response to noradrenaline was unaffected, being 74 .+-. 6.4% of the control.