Abstract

To understand the regulation of rat uterine kallikrein, we evaluated its variations in animals that had been ovariectomized and supplemented with estradiol or progesterone, in pseudopregnant animals intraluminally oil- stimulated or unstimulated, and in unilaterally pregnant animals. The content of kallikrein, determined by an RIA highly specific for rK1 (true tissue kallikrein), rose in ovariectomized rats with estradiol supplementation (0.28 ± 0.03 to 0.44 ± 0.05 ng/mg) and decreased with progesterone (0.13 ± 0.02 ng/mg; n = 15; p < 0.001). Kallikrein content rose from Day 1 of pseudopregnancy (PP1) to a maximum on PP7 (0.18 ± 0.01 to 0.39 ± 0.04 ng/mg protein; n = 36; p < 0.001). On PP7 with unilateral oil intraluminal stimulation, the decidualized horn had higher kallikrein content than did the contralateral (0.98 ± 0.09 vs. 0.35 ± 0.05 ng/mg protein; n = 7; p < 0.001). Immunocytochemistry revealed that mainly rK1 is localized in the luminal and glandular epithelium, and it increased in the stimulated horn. In the unilaterally pregnant rat on Day 7, the fertile horn had a higher kallikrein content than its contralateral control (0.71 ± 0.07 vs. 0.37 ± 0.03 ng/mg protein, p < 0.001; n = 8), as well as a higher kininogenase activity (239 ± 34.3 vs. 83.5 ± 7.9 ng bradykinin(BK)/h per horn, p < 0.003; and 945 ± 90 vs. 585 ± 40 ng BK/h per gram tissue, p < 0.002; n = 6). These results indicate that estrogen stimulates, whereas progesterone inhibits, kallikrein production, and that hormonal regulation is overridden by intraluminal stimulation, thus associating the enzyme with decidualization.