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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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]


  1. 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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