Smith C, Perks A M
Can J Physiol Pharmacol. 1983 Jul;61(7):736-42. doi: 10.1139/y83-114.
Rats with 4-day estrous cycles showed a 51% fall in plasma kininogen in early proestrus (1200-1500). Levels remained depressed throughout ovulation, and then recovered steadily. The initial fall corresponded well with the LH surge. Initial attempts were made to detect enzymes which might be responsible for the change. Kinin-forming enzymes, in either precursor or active forms, were absent from the ovaries in diestrus, but appeared at the onset of the fall in kininogen (kinin-forming activity, 2.87 +/- 0.83 ng bradykinin (BK) equiv. X g wet tissue-1 X min-1). They rose 10-fold just before ovulation, and then declined rapidly. This major peak, and a corresponding one in plasma, may have reflected the presence of follicular proteases. Plasma kinin-forming enzymes showed no apparent change when the kininogen first declined. They then disappeared, suggesting a more delayed activation and destruction. It seems possible that LH induces kinin-forming enzymes in the ovaries, and induces a later activation of plasma enzymes, to produce kinins which may be involved in vascular and permeability changes important in ovulation, and perhaps concerned in the mechanisms of positive feed-back with the pituitary.
具有4天发情周期的大鼠在发情前期早期(1200 - 1500)血浆激肽原水平下降51%。在整个排卵过程中水平持续降低,然后稳步恢复。最初的下降与促黄体生成素(LH)高峰非常吻合。最初尝试检测可能导致这种变化的酶。在动情间期,卵巢中不存在前体或活性形式的激肽形成酶,但在激肽原开始下降时出现(激肽形成活性,2.87±0.83 ng缓激肽(BK)当量×g湿组织-1×min-1)。它们在排卵前上升10倍,然后迅速下降。这个主要峰值以及血浆中的相应峰值可能反映了卵泡蛋白酶的存在。当激肽原首次下降时,血浆激肽形成酶没有明显变化。然后它们消失了,表明激活和破坏更延迟。似乎LH诱导卵巢中的激肽形成酶,并诱导血浆酶的后期激活,以产生可能参与排卵中重要的血管和通透性变化的激肽,并且可能与垂体的正反馈机制有关。