抄録
A role of pituitary on the ovarian estrogen secretion was investigated on the rats hypophysectomized at 1 p.m. in proestrus. The estrogen secretion was minimized within 3hrs. after hypophysectomy. Rat pituitary extract (1 gland e.q.) intravenously injected 2 hrs. after hypophysectomy caused 11 fold increase of estrogen concentration in the ovarian venous blood within 1hr., the extent of which was comparable to that of intact control. Either LH or FSH alone was able to restore the estrogen secretion, and the time required to reach the maximal response was 1hr. for LH and 2hrs. for FSH. In the 1 hr. test, the minimal effective dose for NIH-LH-S3 and NIH-FSH-S1 appeared to be less than 0.25 and 2.5μg per rat, respectively. The total activities of the two preparations to produce estrogen appeared to be the same. Under the same conditions, 10 IU of prolactin slightly stimulated the secretion, whereas 20mU of ACTH was quite negative. These results confirmed pituitary gonadotropin dependency of estrogen secretion from the ovary having ripened follicles. It was further demonstrated that the ovary, after completion of ovulatory surge of LH, abolished its reactivity to the pituitary extract containing a sufficient amount of substance (s) in promoting estrogen secretion. An exogenous LH injected at 11 a.m. of proestrus also caused termination of ovarian estrogen secretion with a time lag of 3hrs., the duration of which was equivalent to the interval between the initiation of ovulatory discharge of LH and termination of estrogen secretion in intact rats. Either NIH-FSH-S4 or NIH-LH-S12 was able to terminate estrogen secretion even at a minute dose as small as 10μg per rat. From these facts, it is considered that both FSH and LH provide a dual effect on ovarian estrogen secretion at the preovulatory stage, promotion and suppression; the former is an acute and direct action of hormones on steroidogenesis and the latter probably a delayed and indirect action of ovulation inducing hormone, the release of which initiates the differentiation of estrogen forming cells towards ovulation unfavorable to estrogen synthesis.
