Effects of nifedipine on contractile responses to potassium, histamine, and 5-hydroxytryptamine in isolated human pulmonary vessels.

Isolated human pulmonary arteries and veins cut to ring preparations responded with maximum contractions to potassium (127 mM; K), histamine (90 microM), and 5-hydroxytryptamine (47 microM; 5-HT). Nifedipine (0.003-3 microM) had a concentration-dependent relaxant effect on contractions induced by K, histamine, or 5-HT. The magnitudes of the relaxant effect of nifedipine were equal in arteries and veins, except in the highest concentrations used, in which case the effect was more pronounced on K-induced contractions in veins than in arteries. The effect of nifedipine was less pronounced on contractions induced by histamine or 5-HT than on K-induced contractions, and was more pronounced on histamine- than on 5-HT-induced contractions. In Ca-free medium, the response to K was nearly abolished in both arteries and veins. When the Ca concentration was increased from 0 to 4 mM without nifedipine, the contractile response to K was completely restored, while in the presence of nifedipine the response to extracellular Ca was nearly abolished in both types of vessel. The results indicate that active tone induced by K in pulmonary vessels is dependent on Ca entry from the extracellular medium. Nifedipine has a relaxant effect on both arteries and veins. In both types of vessel contractions induced by histamine or 5-HT are more resistant to the effect of nifedipine than contractions mediated by depolarization.