Effects of nifedipine on human placental arteries.
Small chorionic plate arteries (outer diameter 600-700 micron) and umbilical arteries were obtained from human placentas following normal vaginal delivery. Tubal vascular preparations were dissected, mounted in organ baths, and isometric tension was recorded. None of the preparations developed spontaneous contractile activity. The course of potassium-induced contractions differed between chorionic and umbilical arteries. The chorionic arteries showed decreased response to 5-hydroxytryptamine (5-HT) as compared to the umbilical arteries, whereas the contractile response to prostaglandin F2 alpha (PGF2 alpha) was equal. In the chorionic arteries, nifedipine effectively inhibited potassium-induced contractions and, at concentrations of 10(-8)-10(-6) M, decreased responses to 5-HT and PGF2 alpha. Removal of extracellular calcium almost abolished the response to high potassium and reduced the response to both PGF2 alpha and 5-HT by 65%. Nifedipine (10(-8) M) significantly reduced, and nifedipine (10(-7) M) almost abolished, the contractile response induced by calcium after K+ (124 mM) depolarization, and in the presence of PGF2 alpha and 5-HT, nifedipine (10(-8)-10(-7) M) effectively depressed the responses to calcium. The results show decreased response to 5-HT with decreasing dimensions of the placental vessels, and suggest that small placental vessels utilize multiple sources of calcium for contractile responses. Nifedipine seems to interfere with some of these mechanisms and clinical use of the drug may imply a decreased fetal placental vascular resistance.