Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 7 instances, cystic ovarian follicles resulted when adrenocorticotropin (ACTH) was administered daily during the follicular phase of the estrous cycle in cows. Two cows given daily injections of hydrocortisone (cortisol) during the follicular phase of the estrous cycle did not develop cystic ovaries. Plasma concentrations of estradiol in cows with induced cystic ovarian follicles were similar to the peak values observed at estrus and were between 6 and 12 pg/ml. Progesterone concentrations in plasma of cows with cystic ovaries were low, between 1 and 2 ng/ml. Ovulation occurred when 2 cows were given human chorionic gonadotropin (HCG) during the period of ovarian cyst development with ACTH administration. Several days of administration of ACTH was required to cause cyst development. Ovulation occurred at the expected time in 1 cow when injections began on day 19, that is, late in the follicular period. In another cow, when treatment was stopped on day 3, after the expected time of estrus a delayed ovulation occurred. In 2 cows with induced cystic ovarian follicles, cyst atresia occurred spontaneously about day 13 to 17 of the cycle. In these cows, new follicular growth and ovulation followed (although delayed in 1 cow). The time of atresia of cystic follicles was not influenced by the intrauterine injection of 10 ml of sterile saline solution on days 8, 9, and 10 in 1 cow. When 5 mg of prostaglandin F2alpha in 10 ml of sterile saline solution was given (uterine injection) in 2 cows on days 8, 9, and 10, cyst atresia occurred earlier than the time of spontaneous atresia. Intrauterine administration of 100 mg of indomethacin in 10 ml of sterile saline solution daily for 13 or 14 days to 2 cows, starting on day 12 or 13 of the cycle, resulted in persistence of the induced cystic ovarian follicles. After cessation of indomethacin treatment, atresia of cysts followed and new follicular growth and ovulation occurred.
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PMID:Steroid concentrations in cows with corticotropin-induced cystic ovarian follicles and the effect of prostaglandin F2alpha and indomethacin given by intrauterine injection. 17 51

Indomethacin administration in late pregnancy prolonged gestation in caged rhesus monkeys and inhibited premature labour and postponed delivery in chronically catheterized monkey fetuses. Chronic indomethacin treatment was associated with a reduction in the urinary excretion of a prostaglandin metabolite, a potent inhibitory effect on myometrial cyclic AMP phosphodiesterase, and severe oligohydramnios in pre-term and post-term fetuses. Experimental anencephaly (functional hypophysectomy) of the rhesus fetus results in lowered concentrations of maternal oestradiol and loss of the precise control of gestational length, with 40% of fetuses delivering beyond term. Corticotropin (ACTH) infused into the fetus results in raised concentrations of fetal and maternal cortisol, progesterone and oestrogens. Progesterone concentrations in peripheral blood apparently have little bearing on uterine quiescence in the rhesus monkey, since the concentrations of progesterone in maternal and fetal blood vary directly with uterine activity. The results of chronic infusion of corticotropin in the fetal monkey support the theory that in the monkey parturition is mediated by increased oestrogen production by the fetoplacental unit and by a rise in the concentrations of oestrone and prostaglandin in the amniotic fluid.
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PMID:Endocrine and pharmacological factors which influence the onset of labour in rhesus monkeys. 20 94

The release of melanocyte-stimulating hormone (MSH) into the medium during incubation and the pituitary tissue content of MSH were measured separately using pituitary glands collected from rats at various stages of the oestrous cycle. The MSH was measured by a biological assay using a synthetic alpha-MSH as standard. The release of MSH was maximal during thepro-oestrous phase and MSH content of the pituitary gland was highest during dioestrus. The influences of the tripeptide Pro-Leu-Gly-NH2, which inhibits MSH secretion in vivo, and of progesterone on the release of MSH in vitro were studied with tissue collected at various phases of the oestrous cycle. Pro-Leu-Gly-NH2 was effective in inhibiting MSH release both at pro-oestrus and oestrus but not at dioestrus. Progesterone overcame this inhibition.
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PMID:Differences in the release of melanocyte-stimulating hormone in vitro by rat pituitary glands collected at various times during the oestrous cycle. 56 39

To investigate the possible involvement of pituitary hormones in the regulation of steroidogenesis during reptilian sexual differentiation, we tested the ability of gonadotropin (ovine FSH), adrenocorticotropin (porcine ACTH), and growth hormone (bovine GH) to stimulate in vitro steroidogenesis in embryonic adrenal-kidney-gonad complexes (AKGs) of a turtle, Trachemys scripta, during and after the temperature-sensitive period for sex determination (TSP). Radioimmunoassays were used to measure progesterone, testosterone, estradiol, and corticosterone in incubation media; additionally, immunoreactive ACTH was measured in plasma. Presumptive male and female AKGs were stimulated by both FSH and ACTH at each stage investigated. Secretion of progesterone and corticosterone was usually far greater than that of testosterone or estradiol in both basal and hormone-stimulated incubations. In general, AKGs from presumptive males secreted more progesterone and corticosterone than AKGs from presumptive females. Progesterone and estradiol secretions were stimulated by both FSH and ACTH, but testosterone secretion was stimulated only by ACTH. Corticosterone secretion was strongly stimulated by ACTH. GH failed to significantly stimulate steroid secretion. Plasma ACTH levels were significantly higher in males than in females, and both sexes had significantly higher plasma levels of ACTH after the TSP compared to during the TSP. Our data demonstrate that during the temperature-sensitive period AKGs are responsive to both gonadotropin and ACTH, and that there are significant sex differences in steroidogenesis, sensitivity to gonadotropin and ACTH, and plasma ACTH levels.
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PMID:Stimulation of in vitro steroidogenesis by pituitary hormones in a turtle (Trachemys scripta) within the temperature-sensitive period for sex determination. 133 78

Progestin receptor-containing cells in the hypothalamus of the adult female green monkey (Cercopithecus aethiops) were examined by double-label immunocytochemical methods to determine their anatomical location, neurotransmitter content and afferent connections. Animals were ovariectomized and administered either estradiol valerate or the oil injection vehicle, and were sacrificed after 10 days of treatment. Using a monoclonal antibody raised against rabbit uterine progestin receptor (PR), the distribution of PR-immunoreactive cells in the mediobasal hypothalamus and the effect of estrogen treatment on this distribution was determined. PR-immunoreactive cells were found throughout the ventromedial nucleus (VMN), in the area between the VMN and fornix, and in the medial portion of the infundibular nucleus. Estrogen treatment dramatically increased both the number of labeled cells and the intensity of immunoreaction product in these regions. In double-immunostained sections, boutons immunoreactive for antigens indicative of serotonin, pro-opiomelanocortin derived peptides, GABA, catecholamine, neuropeptide Y, substance P, cholecystokinin, and somatostatin were demonstrated to establish synaptic contact with the soma of PR-immunoreactive hypothalamic neurons. In colchicine-pretreated animals, all PR-containing neurons in the mediobasal hypothalamus were found to contain immunoreactivity for glutamic acid decarboxylase, the enzyme required for synthesis of GABA. No evidence of colocalization with other antigens, including LHRH, was observed. Because LHRH neurons are known to receive a rich GABAergic innervation PR-containing GABAergic cells may represent steroid-sensitive sites of integration for inputs from other neural systems involved in the control of gonadotropin secretion.
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PMID:Transmitter content and afferent connections of estrogen-sensitive progestin receptor-containing neurons in the primate hypothalamus. 135 61

Immunoreactive beta-endorphin (IR-beta END) is present in human endometrium. Several indirect lines of evidence suggest that endometrial beta END is under steroid hormone control, i.e. IR-beta END is detectable in the secretory, but not the proliferative, endometrium, and progesterone administration increases the concentration of IR-beta END in uterine secretions of ovariectomized gilts. To study the effect of steroid hormones on endometrial beta END, we first questioned whether Ishikawa human endometrial adenocarcinoma cells (which respond to steroid hormones) express the proopiomelanocortin (POMC) gene. Indeed, on Northern blot analysis, a RNA similar or identical in size to pituitary POMC mRNA was present in Ishikawa cell RNA extracts. IR-beta END was also present in Ishikawa cell extracts and culture medium, which coeluted with synthetic human beta END in a Sephadex G-50 column. Ishikawa cells released most of their IR-beta END into the culture medium. Estradiol decreased the release of IR-beta END from Ishikawa cells, an effect that was dependent upon dose and time. The maximal effect was observed after a 4-day exposure to 10 nM estradiol (44 +/- 6% of the control value; n = 6; P less than 0.001). This effect was almost completely counteracted by a 100-fold excess of the antiestrogen 4-hydroxytamoxifen. Progesterone and dihydrotestosterone did not have a statistically significant effect on IR-beta END release. Dexamethasone had effects similar to those of estradiol, i.e. decreased the release of IR-beta END in a time- and dose-dependent manner. The maximal effect was detected after a 4-day exposure to 10 nM dexamethasone (53 +/- 6% of the control value; n = 6; P less than 0.001). Interestingly, the antiprogestin-antiglucocorticoid RU486 exhibited agonistic properties, i.e. diminished the release of IR-beta END in a time- and dose-dependent fashion, possibly via the glucocorticoid receptor. Its maximal effect was reached after a 4-day exposure to 10 nM RU486 (55 +/- 6% of the control value; n = 6; P less than 0.001). In conclusion, our data demonstrate that the release of IR-beta END from Ishikawa cells in culture is inhibited by estradiol and dexamethasone, suggesting that endometrial beta END is under estrogen and glucocorticoid regulation, as is the case with hypothalamic and pituitary POMC-derived peptides. This is the first time that the in vitro release of a peripheral-extracranial POMC-derived peptide has been found to be under the direct control of estrogens and glucocorticoids.
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PMID:Steroid hormones regulate the release of immunoreactive beta-endorphin from the Ishikawa human endometrial cell line. 163 59

Oestrous rats and golden hamsters were anesthetized with pentobarbital, one of the femoral arteries and veins and one of the ovarian veins were cannulated. Blood fractions were collected from the ovary. After the first two fractions synthetic adrenocorticotropic hormone (ACTH) or human chorionic gonadotropin (hCG) was injected i.v. Blood pressures and ovarian blood flow were continuously recorded. Progesterone (P) and oestradiol-17 beta (E2) were determined from the ovarian venous blood by radioimmunoassay (RIA). ACTH induced a temporary elevation in the ovarian blood flow, P and E2 secretion both in rats and hamsters. In rats and hamsters hCG induced a continuous elevation in P secretion but the ovarian blood flow and E2 secretion remained unchanged. Luteal cells from pseudopregnant rats or oestrous hamsters were dispersed with collagenase and incubated with ACTH or hCG. A sample of the cells was preincubated with polymixin-B, indomethacin or ibuprofen. P and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) contents of the medium and cyclic 3,5 adenosine monophosphate (cAMP) content of the cells were determined by RIA. ACTH stimulated the release of 6-keto-PGF1 alpha and the secretion of P from the luteal cells of both species, which was inhibited by indomethacin or ibuprofen, but ACTH did not alter the cAMP content of luteal cells. The polymixin-B prevented ACTH to stimulate P secretion, but it did not elevate the 6-keto-PGF1 alpha release, while the cAMP content of the cells remained unchanged. It is supposed that the polyphosphoinositol-Ca(2+)-protein kinase-C second messenger system is involved in the ACTH induced stimulation of P secretion.
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PMID:Action of ACTH in the luteal ovary. 166 58

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.
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PMID:Progesterone-cortisol interaction in control of renin activity but not aldosterone. 220 Dec 19

Progesterone is a potent hormone acting on the female reproductive tract and influencing a series of other functions. Recent studies revealed a correlation between progesterone and brain neurotransmitters and neuropeptides. Our study evaluated the possible effect of norgestimate, a new progestin, on hypothalamic and pituitary beta-endorphin (B-EP) concentration in castrated female rats. Ovariectomy was performed under ethyl ether anesthesia. Treatment was started 3 weeks after surgery. Norgestimate, estradiol benzoate or norgestimate plus estradiol benzoate were administered. The two steroids were dissolved in sesame oil and injected (s.c.) every day for 2 weeks. Pituitary and hypothalamus B-EP concentrations were measured by radioimmunoassay. Our studies showed that norgestimate increases the pituitary and hypothalamic B-EP concentration in female rats, reaching values higher than controls and estrogen-treated rats. Because B-EP has an important role in reproductive function, both modulating gonadotropin secretion and sexual behavior, the present results lead to the hypothesis that norgestimate affecting B-EP concentrations may influence central functions.
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PMID:Norgestimate increases pituitary and hypothalamic concentrations of immunoreactive beta-endorphin. 253 55

Hypothalamic and pituitary beta-endorphin (B-EP) concentrations are modified by ovariectomy and estrogen treatments, supporting a direct interaction between this peptidergic system and gonadal steroids. Because the use of progestins is becoming even more diffuse in clinical practice, we evaluated the effect of progesterone and of the synthetic progestins medroxyprogesterone acetate (MPA), norethisterone acetate (NET) and desogestrel on the concentration of B-EP in the medial-basal hypothalamus and the anterior and neurointermediate pituitary lobes in ovariectomized rats (OVX), treated or untreated with estradiol benzoate (EB). B-EP concentrations were significantly increased by desogestrel in the anterior lobe and by progesterone, desogestrel and medroxyprogesterone acetate in the neurointermediate lobe. Progesterone and progestins significantly reduced B-EP increase induced by estradiol benzoate in the anterior lobe. Estradiol benzoate treatment did not modify the effect of progesterone and desogestrel on B-EP in the neuro-intermediate pituitary lobe. Norethisterone acetate and progesterone increased B-EP concentrations in the medial-basal hypothalamus, while the other steroids were inactive. In contrast, in the hypothalamus all progestins attenuated the increase of B-EP induced by estradiol benzoate (p less than 0.01). These data indicate that progesterone and progestins modulate the hypothalamic and pituitary B-EP concentrations in concert with estrogens. The capacity of progestins to modify the hypothalamic contents of B-EP may represent one of the mechanisms of action of these steroids in influencing brain function.
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PMID:Progesterone and progestins modulate beta-endorphin concentrations in the hypothalamus and in the pituitary of castrated female rats. 297 69


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