“…During the ' oestrogen surge ', uterine adrena¬ line is markedly reduced. Although adrenaline has been reported to act antagonistic¬ ally to oestrogen (Holden, 1939;Leonard, 1962), we found that oestrogen released adrenaline ( 10 • 3 ng. ) on L3 in the uterus of the untreated pregnant rat.…”
Uterine, ovarian, and hypophysial catecholamines in rats were measured daily during the first 6 days of pregnancy. A marked decrease in uterine adrenaline was observed between L3 and L4 of pregnancy. (L0 was the day when postcoital spermatozoa were observed in the vaginal smear. L1, L2, etc., denote leucocyte type smears.) Daily fluctuations in ovarian catecholamines as well as a rise in hypophysial catecholamines between L2 and L3 followed by a reduction thereafter were observed.The results suggest a correlation between the ' oestrogen surge' on L3 of pregnancy and the reduction of uterine adrenaline and hypophysial adrenaline and noradrenaline. The rise in hypophysial catecholamines was related to the hypothalamic stimulation of hypophysial gonadotrophic activity on L2 of pregnancy.
“…During the ' oestrogen surge ', uterine adrena¬ line is markedly reduced. Although adrenaline has been reported to act antagonistic¬ ally to oestrogen (Holden, 1939;Leonard, 1962), we found that oestrogen released adrenaline ( 10 • 3 ng. ) on L3 in the uterus of the untreated pregnant rat.…”
Uterine, ovarian, and hypophysial catecholamines in rats were measured daily during the first 6 days of pregnancy. A marked decrease in uterine adrenaline was observed between L3 and L4 of pregnancy. (L0 was the day when postcoital spermatozoa were observed in the vaginal smear. L1, L2, etc., denote leucocyte type smears.) Daily fluctuations in ovarian catecholamines as well as a rise in hypophysial catecholamines between L2 and L3 followed by a reduction thereafter were observed.The results suggest a correlation between the ' oestrogen surge' on L3 of pregnancy and the reduction of uterine adrenaline and hypophysial adrenaline and noradrenaline. The rise in hypophysial catecholamines was related to the hypothalamic stimulation of hypophysial gonadotrophic activity on L2 of pregnancy.
“…[The action of the latter is difficult to explain, unless administration of the cholinergic agent caused release of endogenous vasoactive catecholamine (20).] Histamine induced a slight increase in intrauterine pO 2 , perhaps a result of its vasodilating action (21). The rapid dose-dependent nature of these responses indicated a relation between drug action and O 2 tension mediated directly through action on the uterine vasculature.…”
Intrauterine oxygen tension was measured in vivo in the adult virgin rat using an oxygen microelectrode and amplifier assembly coupled with a continuous recording system. Intermittent fluctuations in pO« with varying degrees of regularity were observed. In the uterus of the intact rat the frequency of these alterations and level of average pO> were found to be determined primarily by the patency of the uterine arterioles which supply the capillary network in the endometrium. To only a minor degree did contractile activity of the myometrium affect intrauterine oxygen tension. The topical or intravenous administration of epinephrine hydrochloride or acetylcholine chloride induced vasoconstriction of the arterioles and a decrease in intrauterine pO«. Upon the restoration of blood flow accompanying vasodilation, oxygen tension increased. The topical application of histamine phosphate inci-eased capillary bed engorgement and increased intrauterine pC>2.Following ovariectomy during estrus, average intrauterine oxygen tension increased markedly above estrous levels during the subsequent 5 days. The daily sc injection of estrone (0.5, 1.0 or 5.0 Mg) prevented the post-ovariectomy elevation in average pOs, but had little effect on the rate of pO 2 fluctuation. The administration of progesterone (1.0, 2.0 or 4.0 mg) prevented in part the increase in oxygen tension following ovariectomy, but tended to enhance the rate of fluctuation. The administration of 1.0 /xg estrone and 2.0 mg progesterone together resulted in an average intraluminal pO« level intermediate to and a frequency greater than that obtained with either ovarian steroid alone. It was concluded that the availability of oxygen within the uterus probably is regulated by action of the ovarian steroid hormones on vascular contractility and on metabolic and morphologic changes which affect oxygen availability. {Endocrinology 83: 691, 1968)
“…Holden (6) had suggested in 1939 that estrogen action may be mediated by a histamine-like substance when he found that histamine relieved uterine vasoconstriction produced by a variety of agents. Daily parenteral injections of 200 jug-of histamine for 8 days produced in the vagina of the intact rat a histological picture characteristic of pro-estrus and estrus (7).…”
Solutions of histamine dihydrochloride or of a synthetic histamine releasing agent (Compound 48-80) were introduced into the uterine lumen of adult, castrated rats. Within four hours following administration, increases in water content and changes in gross vascular appearance of the organ were produced which were comparable to the maxima induced by intravenous or intraluminal estrogen for the same period of treatment. Intravenously administered cortisol substantially diminished the hyperemia and water imbibition elicited by 48-80 or by histamine.Two of the 4 structurally interrelated antihistamines tested (Benadryl hydrochloride and Chlor-Trimeton maleate), were effective in blocking estradiolstimulated hydration and hyperemia.These findings are regarded as support for the view that estrogen action, in effecting vasodilation and edema in the rat uterus, is mediated by the local release of histamine. It is proposed that cortisol may antagonize responses to estrogen in the uterus by non-specifically decreasing capillary permeability in that organ. I N EXPERIMENTS reported earlier from this laboratory (1), it was observed that a single intravenous dose of estradiol-17/3 administered to the ovariectomized rat was followed in 4 hours by a decrease in the histamine concentration of the uterus. The loss was determined to be approximately 17% of the basal concentration in the organ and was shown to be neither a consequence of the usual water accumulation nor a reflection of an estrogen-induced acceleration of histaminase activity. In addition, uteri taken from intact animals during periods of high endogenous estrogen secretion exhibited less histamine than those in quiescent states. On the basis of these observations it was proposed that certain early correlates of estrogen stimulation, particularly vasodilation accompanied by increased
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