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 [3H]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 KD of 196.7 nM and a Bmax of 1606 fmol/mg protein. The sodium pump activity was determined from the 86Rb+ 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.[1]References
- Sodium pump activity and contractile effect of ouabain in human placental veins. Marín, J., Fernández-Alfonso, M.S., Sánchez-Ferrer, C.F. Eur. J. Pharmacol. (1991) [Pubmed]
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