SODIUM-PUMP ACTIVITY AND CONTRACTILE EFFECT OF OUABAIN IN HUMAN PLACENTAL VEINS

The aim of the present study was to determine the number and affinity of [H-3]ouabain binding sites, the sodium pump activity and the mechanisms involved in the contractile effects of ouabain in human placental veins. Scatchard analysis suggested the existence of a single population of binding sites with a K(D) of 196.7 nM and a B(max) of 1606 fmol/mg protein. The sodium pump activity was determined from the Rb-86+ uptake, which was reduced concentration dependently by ouabain (10(-8)-10(-4) M), and from the K+ (7.5 mM)-induced relaxation in veins preincubated in a K+-free medium and precontracted with PGF2-alpha (10(-6) M), which was also blocked by the glycoside (10(-6) M). Ouabain (10(-7)-10(-4) M) induced concentration-dependent contractions, which were not modified by either nifedipine or Bay K 8644 (10(-7) and 10(-6) M). Ca2+ omission from the medium or amiloride (10(-4) M) inhibited these contractions, whereas monensin (10(-6) M) potentiated them. These data indicate that human placental veins possess sodium pump activity and that its inhibition by ouabain induces potent contractions mainly mediated by Ca2+ entry through the Na+-Ca2+ exchange system.