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Prostaglandin E and F Receptor Expression and Myometrial Sensitivity at Labor Onset in the Sheep¹

Department of Physiology,³ Monash University, Victoria 3800, Australia Prince Henry's Institute of Medical Research,⁴ Clayton, Victoria 3168, Australia Department of Obstetrics and Gynecology,⁵ University of Melbourne, Mercy Hospital for Women, East Melbourne, Victoria 3002, Australia

Prostaglandins (PGs) play a pivotal role in the initiation and progression of term and preterm labor. Uterine activity is stimulated primarily by PGE₂ and PGF₂ acting on prostaglandin E (EP) and prostaglandin F (FP) receptors, respectively. Activation of FP receptors strongly stimulates the myometrium, whereas stimulation of EP receptors may lead to contraction or relaxation, depending on the EP subtype (EP1–4) expression. Thus, the relative expression of FP and EP1–4 may determine the responsiveness to PGE₂ and PGF₂. The aims of this study were to characterize the expression of EP1–4 and FP in intrauterine tissues and placentome, together with myometrial responsiveness to PG, following the onset of dexamethasone-induced preterm and spontaneous term labor. Receptor mRNA expression was measured using quantitative real-time polymerase chain reaction using species-specific primers. There was no increase in myometrial contractile receptor expression at labor onset, nor was there a change in sensitivity to PGE₂ and PGF₂. This suggests expression of these receptors reaches maximal levels by late gestation in sheep. Placental tissue showed a marked increase in EP2 and EP3 receptor expression, the functions of which are unknown at this time. Consistent with previous reports, these results suggest that PG synthesis is the main factor in the regulation of uterine contractility at labor. This is the first study to simultaneously report PG E and F receptor expression in the key gestational tissues of the sheep using species-specific primers at induced-preterm and spontaneous labor onset.

¹ Supported by project grant 194423 from the National Health and Medical Research Council of Australia.

² Correspondence: Hannah K. Palliser, Department of Physiology, Building 13F, Monash University, Victoria 3800, Australia. FAX 61 03 9905 2547; hannah.palliser{at}med.monash.edu.au

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