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Local interaction of prostaglandin F₂ with endothelin-1 and tumor necrosis factor- on the release of progesterone and oxytocin in ovine corpora lutea in vivo: a possible implication for a luteolytic cascade

¹ The Field Center of Animal Science and Agriculture and ² Department of Agriculture and Life Science, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan and ³ Department of Animal Science, University of Peradeniya, Peradeniya, Sri Lanka

Correspondence should be addressed to A Miyamoto; Email: akiomiya{at}obihiro.ac.jp

Endothelin-1 (ET-1) and tumor necrosis factor- (TNF) participate in the cascade of luteolysis. Thus, in the present study the interactions of ET-1 and TNF with prostaglandin F₂ (PGF₂) on the release of progesterone and oxytocin (OT) within the corpus luteum (CL) were investigated. A microdialysis system (MDS) was surgically implanted in ovine CL (one MDS line/CL; 5–10 lines/ewe) formed after super-ovulation. A 4-h perfusion with PGF₂ (0.01–1 µmol l ^-1) induced no clear effect on progesterone release, but acutely stimulated OT release in a dose-dependent manner. A perfusion of PGF₂ (1 µmol l ^-1) increased ET-1 release over a period of 12 h. Two perfusions of ET-1 (0.1 µmol l^-1) or a perfusion of ET-1 followed by TNF (200 ng ml^-1) decreased progesterone release (56–64% at 36–48 h). When the CL were pre-perfused with PGF₂ (1 µmol l^-1), two consecutive perfusions of ET-1 decreased progesterone release more rapidly. Similarly, a pre-perfusion with PGF₂ followed by consecutive perfusions of ET-1 and then TNF rapidly decreased progesterone release, with the inhibition most pronounced (35%) at 36–48 h. The simultaneous infusion of ET-1 with PGF₂ induced a rapid decrease in progesterone release (36% at 36–48 h). In a further study, the possible second messenger systems involved in PGF₂ action on the release of progesterone, OT and ET-1 were investigated. A perfusion with 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 10 µmol l^-1), A23187 (10 µmol l^-1), or PGF₂ + A23187 increased progesterone release during infusion, but decreased it after perfusion. All treatments induced a massive release of OT during infusion, and increased ET-1 release after infusion. These results show that ET-1 is capable of suppressing progesterone release in the PGF₂-primed ovine CL in vivo and thus ET-1 works as a local luteolysin together with PGF₂ during the process of functional luteolysis. During structural luteolysis, TNF may interact with PGF₂ and ET-1 to cause a rapid drop in progesterone release and accelerate the process of luteolysis. This result supports the contention that ET-1 and TNF interact with PGF₂ as local luteolytic mediators in the ewe as previously suggested.

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