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

Effect of the non-peptide, vasopressin V1a receptor antagonist, SR 49059 and its enantiomer, SR 49770, on isolated human myometrium.

BACKGROUND. Vasopressin seems to be an important etiological factor for the myometrial hyperactivity and reduced blood flow in primary dysmenorrhea. Substances which block the action of vasopressin on the uterus are therefore of interest. METHODS. The effect of an orally active, non-peptide vasopressin V1a receptor antagonist, SR 49059, as well as its enantiomer, SR 49770, which is 50 to 100 fold less potent in binding studies, were tested in vitro on myometrium from 14 subjects. Two doses of the compounds, 2 nmol/L and 10 nmol/L, were used for counteracting the contractile effect of arginine vasopressin in a concentration of 0.7 nmol/L. RESULTS. SR 49059, in the lower concentration, significantly decreased the response to arginine vasopressin, measured as area under the recording curve, to 48 per cent of that to the agonist alone, and in the higher dose to 28 per cent. SR 49770 was much less potent in reducing the response to vasopressin. CONCLUSION. The myometrial action of arginine vasopressin is exerted via V1a receptors. The potent stereospecific inhibitory effect of SR 49059 on arginine vasopressin-induced myometrial activity indicates that the compound acts specifically through V1a receptors and may have a therapeutic potential in primary dysmenorrea.[1]

References

  1. Effect of the non-peptide, vasopressin V1a receptor antagonist, SR 49059 and its enantiomer, SR 49770, on isolated human myometrium. Bossmar, T., Rasmussen, T., Akerlund, M. Acta obstetricia et gynecologica Scandinavica. (1996) [Pubmed]
 
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