Abstract
The corpus luteum (CL) of the estrous cycle in the cow is a dynamic organ with a lifetime of approximately 17-18 days. In other words, the CL regresses within a few days when pregnancy does not occur successfully. There is universal agreement that prostaglandin F2α (PGF2 α) is a physiological luteolysin in the cow. Nevertheless, cellular and molecular mechanisms involved in local actions of PGF2α in the CL have not been fully elucidated. Recent observations suggest that the endothelial cell-derived vasoconstrictive peptide endothelin-l (ET-l) interacts with PGF2α, and that luteal ET-l participates in the rapid cascade of functional luteolysis in vivo. In the bovine CL, ET-l inhibits P secretion in luteal cells in culture and in the in vitro microdialysis system (MDS) of luteal explants. Moreover, PGF2α stimulates ET-l secretion in this MDS. Further in vivo observation confirmed that PGF2α injection rapidly increased ET-l release within the regressing CL as well as into the ovarian venous blood in the cow. All these findings strongly suggest a physiological impact of PGF2α and ET-l in the acute depletion of blood flow into the CL and the rapid cascade of functional luteolysis in vivo, and thus a possible interaction between endothelial cells and luteal cells during luteolysis. Overall results strongly support the hypothesis that luteal ET-l is a local luteolytic mediator/promotor in the regressing bovine CL.
