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The corpus luteum (CL) of ruminants exhibits periods of reduced sensitivity to the luteolysin prostaglandin F2α (PGF2α). The CL has reduced sensitivity to PGF2α early in the luteal phase. Mechanisms of reduced luteal sensitivity to PGF2α during the early portion of the luteal phase have been widely studied, with a focus on regulation of cyclooxygenase-2 and components of the endothelin system. The first ovulation in postpartum cows results in a CL that regresses during transition from a period of reduced sensitivity to susceptibility to PGF2α, and there is evidence that the first CL in the postpartum cow is more sensitive to PGF2α. Corpora lutea are less sensitive to PGF2α during the maternal recognition of pregnancy. In the ewe, studies were performed to quantify mRNA for prostaglandin metabolic enzymes and components of the endothelin system, as well as catabolism of PGF2α to inactive PGFM in CL expected to regress early in postpartum cows and in pregnant ewes expected to have CL that do not regress after an injection of PGF2α. In both experiments, transcription of enzymes involved in prostaglandin anabolism were regulated by the abundance of PGE synthase and PGF synthase mRNA instead of cyclooxygenase-2 mRNA. Catabolism of PGF2α to PGFM was regulated post-transcriptionally. It was also demonstrated that the endothelin system may contribute to reduced luteal sensitivity to PGF2α through alterations in the endothelin converting enzyme-1 mRNA instead of alterations in the abundance of preproendothelin-1 or endothelin receptor type A mRNA. In conclusion, the early regressing CL in the postpartum cow did not appear to differ from non-regressing CL with respect to PGE synthesis or PGF2α catabolism. Nevertheless, premature uterine secretion of PGF2α activates mediators of regression. In pregnant ewes, the conceptus, which alters uterine secretion of prostaglandins to a greater ratio of PGE2: PGF2α, may cause a similar shift in prostaglandin production in the CL to a greater ratio of PGE2: PGF2α, a reduction of endothelin converting enzyme-1, and greater catabolism of PGF2α to the inactive metabolite PGFM.