Due to the similarity between events of an inflammatory response and ovulation, this investigation was conducted to evaluate the involvement of the kinin system in the cascade of events that leads to ovulation. PMSG/hCG primed immature 23-day-old female rats were used for evaluation of ovulation, ovarian steroid levels, and changes in the levels of kinin system components. Kininogens and kallikrein were present in the ovary and their levels changed significantly during ovulation. Increases in ovarian total kininogen levels occurred at 10 h and 30 h after hCG. These increases were mainly due to an elevation in T-kininogen, an acute phase protein and the predominant species of kininogen in the ovary. On the other hand, at 10 h after hCG, a time immediately prior to ovulation, low molecular weight kininogen decreased, as compared with 0 h. This suggests that low molecular weight kininogen may be metabolized by kallikrein to produce bradykinin prior to and during ovulation. T-kininogenase, the enzyme which releases T-kinin from T- kininogen, was not detectable in the ovary during ovulation. Therefore, along with the evidence that ovarian cathepsin B activity was suppressed at 10 h, the time when T-kininogen levels increased significantly, T-kininogen may remain in its intact form to exert its function as an proteinase inhibitor. The regulation of the kinin system in the ovary during ovulation is not very clear; however, the administration of an antiprogestin compound, RU 486, did not alter the increase in ovarian kininogen level which preceded ovulation. Interestingly, the second rise of ovarian kininogen (at 30 h) was augmented by RU 486 treatment. Apparently, the changes in ovarian kininogen during ovulation were regulated by some system other than progesterone. Prolactin stimulates T-kininogen production in hepatocytes in vitro and RU 486 enhances prolactin release. The study of the relationship between serum prolactin and ovarian T-kininogen levels in the RU 486-treated PMSG/hCG-primed rats showed that, as compared with the vehicle group, the RU 486-treated group demonstrated an increase in serum prolactin levels at 30 h after hCG which paralleled the changes in T-kininogen levels. It would appear that prolactin may be one of the modulators responsible for the changes of T-kininogen in the ovary by RU-486. In conclusion, the components of the kinin-kininogen- kallikrein system are present in the ovary; their concentrations undergo significant changes during ovulation. At 10 h after hCG, a time immediately preceding ovulation, low molecular weight kininogen may be cleaved by kallikrein to release bradykinin while T-kininogen, the major species of kininogen in the ovary, remains intact as a proteinase inhibitor. The rise of both low molecular weight kininogen and T-kininogen at 30 h after hCG suggests involvement of kinin system in formation of corpus luteum. The increase in T-kininogen by RU 486 at 30 h after hCG was regulated by prolactin. Ovulation is indeed an inflammatory-type response and the kinin system is an important mediator of the ovulatory process.
|Original language||English (US)|
|Number of pages||7|
|Journal||Advances in Contraceptive Delivery Systems|
|State||Published - Dec 1 1993|
ASJC Scopus subject areas
- Obstetrics and Gynecology