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Administration of Prostaglandin F₂ During the Early Bovine Luteal Phase Does Not Alter the Expression of ET-1 and of Its Type A Receptor: A Possible Cause for Corpus Luteum Refractoriness

^a Department of Animal Science, Faculty of Agriculture, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel ^b Department of Animal Science, Obihiro University of Agriculture & Veterinary Medicine, Obihiro 080-8555, Japan

ABSTRACT

Luteal regression is initiated by prostaglandin F₂ (PGF₂). In domestic species and primates, demise of the corpus luteum (CL) enables development of a new preovulatory follicle. However, during early stages of the cycle, which are characterized by massive neovascularization, the CL is refractory to PGF₂. Our previous studies showed that endothelin-1 (ET-1), which is produced by the endothelial cells lining these blood vessels, plays a crucial role during PGF₂-induced luteolysis. Therefore, in this study, we compared the effects of PGF₂ administered at the early and mid luteal phases on ET-1 and its type A receptors (ETA-R) along with plasma ET-1 and progesterone concentrations, and the mRNA levels of PGF₂ receptors (PGF₂-R) and steroidogenic genes. As expected, ET-1 and ETA-R mRNA levels were markedly induced in midcycle CL exposed to luteolytic dose of PGF₂ analogue (Cloprostenol). In contrast, neither ET-1 mRNA nor its receptors were elevated when the same dose of PGF₂ analogue was administered on Day 4 of the cycle. In accordance with ET-1 expression within the CL, plasma ET-1 concentrations were significantly elevated 24 h after PGF₂ injection only on Day 10 of the cycle. The steroidogenic capacity of the CL (plasma progesterone as well as the mRNA levels of steroidogenic acute regulatory protein and cytochrome P450_scc) was only affected when PGF₂ was administered during midcycle. Nevertheless, PGF₂ elicited certain responses in the early CL: progesterone and oxytocin secretion were elevated, and PGF₂-R was transiently affected. Such effects probably result from PGF₂ acting on luteal steroidogenic cells. These findings may suggest, however, that the cell type mediating the luteolytic actions of PGF₂, possibly the endothelium, could yet be nonresponsive during the early luteal phase.

FOOTNOTES

First decision: 12 November 1999.

¹ Correspondence. FAX: 972 8 9465763; rina{at}agri.huji.ac.il

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