Regulatory factors for luteolysis in ruminants

In ruminants, there is clear evidence that luteal regression at the end of the oestrous cycle is caused by episodic release of prostaglandin F_2α (PGF_2αJ from the uterus. Experiments demonstrate that exposure to physiological luteal progesterone levels or inhibition of progesterone receptors by antagonist regulates the onset of uterine release of PGF2α pulses for induction of luteolysis, and causes shortening or extension of the interoestrous interval in sheep and cows. There is strong support that vasoconstrictive peptides may play a key role during the luteolytic cascade. Therefore we investigated in detail the real-time changes (corpora lutea were collected before and 2, 4, 12, 24, 48 and 64 h (n=5/phase) after PG analogue injection) in mRNA expression of angiotensin-converting enzyme (ACE), angiotensin-receptors (ATR-1 and ATR-2), endothelin-1 (ET-1), ET receptors (ETR-A and ETR-B), and measured luteal tissue concentrations of angiotensin II (Ang II) and ET-1. ACE and ET-1 mRNA expression and Ang II and ET-1 tissue concentrations increased continuously to maximum levels 24 - 48 h after PG analogue injection and declined thereafter. ETR-A and ETR-B mRNA levels show a similar trend. The ATR-1 mRNA is unchanged and ATR-2 increased after 48 and 64 h. Thus, we propose that PGF_2α administration triggers Ang II and ET-I release in corpus luteum (CL), which causes functional luteolysis by suppression of progesterone production and release by vasoconstriction of arteriols and direct effects on luteal cells.