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Effect of Oxytocin Receptor Blockade on Rat Myometrial Responsiveness to Prostaglandin F₂¹

^a Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhagen, Denmark ^b Department of Medical Physiology, The Panum Institute, University of Copenhagen, Denmark

ABSTRACT

In the present study we have shown that the genetic expression of prostaglandin (PG)F₂ receptor (R) and cyclooxygenase (COX)-2 increases in laboring rat myometrium. This finding was associated with a relatively weak contractile in vitro response (E_max) of isolated uterine strips when challenged with PGF₂. Five days postpartum PGF₂-R mRNA values exceeded those during labor while COX-2 mRNA was reduced to preparturient values. Maximal contractility of isolated strips stimulated with PGF₂ at this time was enhanced and EC₅₀ decreased. Oxytocin treatment of estrogen-primed nonpregnant rats down-regulated uterine contractile responsiveness to PGF₂, leaving mRNA values for this receptor unchanged, whereas oxytocin receptor blockade with atosiban (an oxytocin receptor antagonist) left E_max unaltered. In contrast, atosiban treatment of pregnant rats resulted in a 2.5-fold increase in E_max and a considerably reduced EC₅₀ during labor when compared to untreated delivering rats. The increased contractile ability was associated with a threefold increase in PGF₂-R mRNA production, indicating that the regulation by atosiban of the PGF₂-induced response is exerted at the genetic level. Based on the present data we suggest that 1) PGF₂-R stimulation may not primarily exert a contracting role in the normally delivering myometrium, and 2) the presence of the PGF₂-R system in rat myometrium may explain the apparent functional redundancy of the oxytocinergic system during the process of birth in animals lacking oxytocin or where the oxytocin receptor is blocked. In this context PGF₂ receptor stimulation may, in the absence of oxytocin receptor stimulation, exert the contractile forces needed for proper propulsion of the fetus.

FOOTNOTES

First decision: 28 February 2000.

¹ The present study was supported by The Danish Biotechnology Program, The Danish Medical Research Council, The Novo Nordisk Foundation, Jacob Madsen & Hustru Olga Madsens Foundation, The Danish Medical Association Research Fund, Foundation Idella, The Dagmar Marshall Foundation, Direktør E. Danielsen og Hustrus Foundation, and Ove Villiam Buhl Olesen & ægtefælle Edith Buhl Olesens Foundation.

² Correspondence: Thomas Engstrøm, Department of Medical Physiology 12.2.39, The Panum Institute, University of Copenhagen, Copenhagen, Denmark. FAX: 45 35327537; engstrom{at}mfi.ku.dk

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