Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
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

Parturition in sheep is initiated by a sharp rise in the rate of secretion of cortisol by the fetal adrenal. Increased secretion is due partly to enhanced responsiveness to corticotropin (ACTH) and partly to increased fetal concentrations of corticotropin. Cortisol acts on placental enzymes active in the biosynthesis of oestrogens from progesterone. Thus placental secretion of oestrogen increases and that of progesterone decreases. This change in the ratio of oestrogen: progesterone, particularly the rise in oestrogen, stimulates release of prostaglandin F2alpha (PGF2alpha) from the maternal placenta and to a lesser extent from the myometrium. PGF2alpha enhances the myometrial response to oxytocin and, after a latent period, stimulates contractions. The onset of parturition is normally associated with softening of the cervix, the mechanism of which is uncertain. Uterine contractions in the presence of a distensible cervix lead to parturition.
 ...
PMID:Parturition in the sheep. 20 98

The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and beta-endorphin-like immunoreactivity (beta-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2.8 and 28 mumol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of beta-EI was enhanced by indomethacin (28 mumol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of beta-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 mumol/l). Prostaglandin F2 alpha (5 mumol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 mumol/l) did not. Prostaglandin F2 alpha (5 mumol/l), D2 and I2 (1.5 mumol/l each) produced no effects on beta-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of beta-EI and, as can be inferred, alpha-MSH, by a direct action on intermediate lobe cells.
 ...
PMID:Inhibition by prostaglandin E2 of the release of vasopressin and beta-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro. 316 Aug 2