5-Hydroxytryptamine (5-HT) and K+ induced contractions in human chorionic arteries and veins. 5-HT-caused responses were blocked by ketanserin (10(-7) and 10(-6) M) and prazosin (10(-5) but not 10(-6) M). K(+)-induced contractions were practically abolished in a Ca2(+)-free medium, whereas those produced by 5-HT were reduced. The efficacy (EC50 values) of diltiazem to produce relaxation in arteries and veins contracted with 40 or 75 mM K+ was similar, but normally greater than that of nifedipine. The potency of nifedipine (IC50 values) to inhibit maximal K+ contractions was greater than to inhibit maximal 5-HT contractions; diltiazem showed an inverse order of potency, which was less than that of nifedipine. The time course of 10(-6) M 5-HT and 75 mM K+ contractions was different, as much in the absence as in the presence of both Ca2+ antagonists; 5-HT contractions were transient, but sustained those elicited by K+. K+ (75 mM) and 5-HT (10(-6) M) produced increases in 45Ca2+ uptake, which were reduced by the Ca2+ antagonists. These results indicate that (a) human chorionic arteries and veins are similarly sensitive to Ca2+ antagonists, (b) 5-HT-induced contractions were largely dependent on extracellular Ca2+ and mainly mediated by 5-HT2 receptors but not by alpha 1-adrenoceptors, and (c) nifedipine was more potent than diltiazem in inhibiting Ca2+ influx through potential- and receptor-dependent Ca2+ channels.