Estradiol levels near the time of ovulation in the bonnet monkey (Macaca radiata)

Plasma estradiol-17beta and total progestins were determined to delineate the relationship between preovulatory estradiol-17beta peak and ovulation in the bonnel monkey (Macaca radiata). 6 monkeys were studied for 15 menstrual cycles. In subsequent cycles, serial laparotomy was performed in 5 of the 6 monkeys to correlate ovarian morphology to plasma estradiol-17beta. In 11 of the 15 cycles, estradiol-17beta peaks were 3- to 7-fold above baseline levels near the time of expected ovulation (Cycle Days 7-12). Plasma progestin rose significantly from follicular phase levels of .5 ng/ml to 2.6 ng/ml the day of the estradiol-17beta peak with peak levels of 4.5 ng/ml on the following day. Ovarian morphology in 4 of the 5 observed by laparotomy demonstrated ovulation within 48 hours following an estradiol-17beta peak of approximately 300 pb/ml.     

Serum estradiol-17beta concentrations during spontaneous silent estrus and after prostaglandin treatment in the mare

Serum estradiol-17beta concentrations were determined during silent estrus in the mare. Relationships between serum estradiol-17beta concentration, corpus luteum regression, follicular development, ovulation, prostaglandin treatment and behavioral estrus were investigated. The expression of behavioral estrus was found to be related to the patterns of progesterone and estradiol-17beta secretion during the periovulatory period. When compared to normal estrous cycles, silent estrus was accompanied by a significantly lower maximum serum estradiol-17beta concentration (47.8 vs 34.6 pg/ml), a significantly longer interval from maximum estradiol-17beta concentration to ovulation (1.7 vs 4.0 days), and a significantly shorter interval from corpus luteum regression to ovulation (5.3 vs 2.8 days). Silent estrus following prostaglandin treatment was related to a significantly shorter interval from prostaglandin treatment to ovulation (3.6 +/- 0.4 days) than from normal corpus luteum regression to ovulation (5.3 +/- 0.3 days). Silent estrus appeared to be related to changes in follicular estradiol-17beta secretion and to the pattern of its secretion as related to regression of the corpus luteum. There appeared to be not only less estradiol-17beta present, but also less time available after luteal regression for it to interact with the central nervous system to elicit the changes necessary to cause behavioral estrus. There fore, unusual relationships between luteal function and folliculogenesis can result in one type of silent estrus. Significant correlations (P<0.05) were found between follicle size and serum estradiol-17beta concentration whenever behavioral estrus occurred [follicle diameter in mm = 0.96 (serum estradiol-17beta in pg/ml) + 6.08 and 0.73 (serum estradiol-17beta + 13.32 for control and normal estrus following prostaglandin treatment groups, respectively]. During silent estrus, however, no significant correlations between follicle size and serum estradiol-17beta concentration were observed.     

Steroids and follicular rupture at ovulation

The preovulatory surge of gonadotropins stimulates follicular steroidogenesis and changes from estrogen as the major product to progesterone. We shall overview the studies dealing with the role of ovarian steroidogenesis in follicular rupture at ovulation. Several inhibitors of steroidogenesis blocked follicular rupture in vivo. Likewise, RU 38486 partially blocked ovulation triggered by hCG. Collectively, these data support the knowledge that follicular steroidogenesis is required for ovulation. Recent studies confirmed the essential role of plasminogen activator (PA) in follicular rupture. The LH stimulation of PA activity was partially blocked by several inhibitors of steroidogenesis and it could be restored by the addition of progesterone, testosterone and estradiol-17 beta, but not the non-aromatizable 5 alpha-dihydrotestosterone. Gonadotropic stimulation enhanced only the synthesis of tissue type PA (t-PA) and not that of urokinase. Likewise, inhibition of steroidogenesis, reduced only the synthesis of t-PA and was reversed by addition of estradiol-17 beta. It seems, therefore, that follicular steroids, most probably estrogen, are involved in the preovulatory rise in follicular t-PA activity.     

Ovarian function in Nelore (Bos taurus indicus) cows after post-ovulation hormonal treatments

Maternal recognition of pregnancy in the cow requires successful signaling by the conceptus to block luteolysis. Conceptus growth and function depend on an optimal uterine environment, regulated by luteal progesterone. The objective of this study was to test strategies to optimize luteal function, as well as prevent a dominant follicle from initiating luteolysis. Nelore (Bos taurus indicus) beef cows (n=40) were submitted to a GnRH/PGF(2alpha)/GnRH protocol. Cows that ovulated from a dominant ovarian follicle (ovulation=Day 0) were allocated to receive: no additional treatment (G(C); n=7); 3000IU of hCG on Day 5 (G(hCG); n=5); 5mg of estradiol-17beta on Day 12 (G(E2); n=6); or 3000IU of hCG on Day 5 and 5mg of estradiol-17beta on Day 12 (G(hCG/E2); n=5). Ultrasonographic imaging of the ovaries, assessment of plasma progesterone concentration, and detection of estrus were done daily from Day 5 to the day of subsequent ovulation. Treatment with hCG induced an accessory CL, increased CL volume, and plasma progesterone concentration throughout the luteal phase (P<0.01). Estradiol-17beta induced atresia and recruitment of a new wave of follicular growth; it eliminated a potentially estrogen-active, growing ovarian follicle within the critical period for maternal recognition of pregnancy, but it also hastened luteolysis (Days 16 or 17 vs. Days 18 or 19 in non-treated cows). In conclusion, the approaches tested enhanced luteal function (hCG) and altered ovarian follicular dynamics (estradiol-17beta), but were unable to extend the life-span of the CL in Nelore cows.     

Effects of catecholamines on ovary morphology, blood concentrations of estradiol-17beta, progesterone, zinc, triglycerides and rate of ovulation in domestic hens

The present study is an attempt to shed more light on the role of epinephrine (EP) and norepinephrine (NE) in regulating ovarian follicular development, folliculogenesis and ovulation in laying hens. Sixty Egyptian local cross females (Mandarah), 50 weeks old, were individually housed and equally divided into three treatments: control (saline, 0.9% NaCl), EP (0.15 mg epinephrine/hen/day) and NE (0.75 mg norepinephrine/hen/day) (n=20). Animals were injected intramuscularly once a day for 15 successive days. At the end of the experimental period, 10 females from each treatment were randomly chosen, weighed and killed by decapitation. Ovaries and oviducts and ovarian follicles were examined. Plasma concentrations of estradiol-17beta, progesterone, zinc and triglyceride were determined. Results indicated that the ovaries of NE- and EP-treated hens were more developed than those of control hens being heavier and containing more yellow yolk-filled follicles. EP or NE significantly increased the ovulation rate and plasma concentrations of estradiol-17beta, progesterone, zinc and triglyceride compared with control treatment. It could be concluded that catecholamines may have a part in promoting ovarian follicular development and in stimulating ovulation in laying hens at the end of their reproductive lives.     

Evidence for a decrease in aromatase activity in the ovarian granulosa cells of amago salmon (Oncorhynchus rhodurus) associated with final oocyte maturation

Aromatase activity in the isolated granulosa layers of amago salmon (Oncorhynchus rhodurus) ovarian follicles was examined during the course of vitellogenesis and final oocyte maturation and ovulation. Estradiol-17 beta production by isolated granulosa layers incubated with exogenous testosterone increased during the period of vitellogenesis to reach a peak in late vitellogenesis, and then declined rapidly, in association with the ability of the oocyte to mature in response to partially purified salmon gonadotropin (SG-G100). Extremely low levels of estradiol-17 beta were produced by granulosa layers from follicles which had undergone final oocyte maturation in vivo and by post-ovulatory follicles. SG-G100 had no discernible effect on estradiol-17 beta production. These results are discussed in relation to other studies on the endocrine control of steroidogenesis in this species.     

Reproductive hormones associated with the ovarian cyst response to GnRH

Eighteen cows with ovarian cysts were administered 100 mug of GnRH and bled prior to treatment, at half hour intervals for 4 hours posttreatment and on days 1, 5 and 9 posttreatment. Blood plasma was analyzed for estradiol-17beta, progesterone and LH by radioimmunoassay. Response to treatment was recorded as positive if ovulation was detected within 30 days posttreatment. Fourteen cows (78%) initiated ovarian cycles by 30 days posttreatment. Mean pretreatment concentrations of estradiol-17beta, progesterone and LH and the GnRH induced LH release were not different for positive or no response cows. However, all seven cows that had pretreatment progesterone concentrations greater than 1.0 ng/ml had a positive response to treatment. Eight of the remaining eleven cows had a progesterone response (mean progesterone concentrations on days 5 and 9 posttreatment) greater than 1.0 ng/ml; seven had a positive response to treatment. In summary, most cows with ovarian cysts administered GnRH will initiate ovarian cycles within 30 days if: 1) pretreatment progesterone concentrations are greater than 1.0 ng/ml or 2) if progesterone response is greater than 1.0 ng/ml.     

Synchronization of follicular wave emergence in the seasonally anestrous ewe: the effects of estradiol with or without medroxyprogesterone acetate

Fertility is often lower in anestrous compared to cyclic ewes, after conventional estrus synchronization. We hypothesized that synchronization of ovarian follicular waves and ovulation could improve fertility at controlled breeding in anestrous ewes. Estradiol-17beta synchronizes follicular waves in cattle. The objectives of the present experiments were to study the effect of an estradiol injection, with or without a 12-d medroxyprogesterone acetate (MAP) sponge treatment, on synchronization of follicular waves and ovulation in anestrous ewes. Twenty ewes received sesame oil (n=8) or estradiol-17beta (350 microg; n=12). Eleven ewes received MAP sponges for 12d and were treated with oil (n=5) or estradiol-17beta (n=6) 6d before sponge removal. Saline (n=6) or eCG (n=6) was subsequently given to separate groups of ewes at sponge removal in the MAP/estradiol-17beta protocol. Estradiol treatment alone produced a peak in serum FSH concentrations (4.73+/-0.53 vs. 2.36+/-0.39 ng/mL for treatment vs. control; mean+/-S.E.M.) after a short-lived (6 h) suppression. Six of twelve ewes given estradiol missed a follicular wave around the time of estradiol injection. Medroxyprogesterone acetate-treated ewes given estradiol had more prolonged suppression of serum FSH concentrations (6-18 h) and a delay in the induced FSH peak (32.3+/-3.3 vs. 17.5+/-0.5 h). Wave emergence was delayed (5.7+/-0.3 vs. 1.4+/-0.7d from the time of estradiol injection), synchronized, and occurred at a predictable time (5-7 vs. 0-4d) compared to ewes given MAP alone. All ewes given eCG ovulated 3-4d after injection; this predictable time of ovulation may be efficacious for AI and embryo transfer.     

Insulinotropic effect of ovarian steroid hormones in streptozotocin diabetic female mice

To investigate the protective effect of ovarian sex steroids against streptozotocin diabetes, groups of ovariectomized streptozotocin diabetic female mice were treated orally with estradiol-17 beta (5 and 500 ug/kg/day) or progesterone (1 mg/kg/day) for 10 weeks. Streptozotocin produced a more severe hyperglycaemia and a greater fall in plasma insulin concentrations in ovariectomized mice than intact female mice. The estradiol-17 beta and progesterone treatments reduced both the severity of the hyperglycaemia and the fall in plasma insulin. Loss of pancreatic insulin after streptozotocin administration was reduced in intact mice and in mice treated with estradiol-17 beta. These observations suggest that ovarian sex steroids reduce the severity of streptozotocin diabetes at least partly by countering the cytotoxic effect of the drug on the islet B-cells, thereby reducing the fall in pancreatic and plasma insulin.     

Effect of various agents on ovarian plasminogen activator activity during ovulation in pregnant mare's serum gonadotropin-primed immature rats

The plasminogen activator/plasmin synthetic substrate S-2251 was used to measure the effect of indomethacin, cycloheximide, colchicine, dexamethasone, tranexamic acid, and aprotinin on the elevation of ovarian plasminogen activator (PA) that normally occurs during ovulation in the rat. Young Wistar rats were weaned on the morning of Day 21, given 4.0 IU of pregnant mare's serum gonadotropin (PMSG) s.c. at 0800 h on Day 22, and given 10.0 IU of human chorionic gonadotropin (hCG) on Day 24. These animals normally began ovulating between 0000 and 0200 h on Day 25. The induced ovulation rate was 11.5 +/- 2.2 ova/rat, based on the number of ova in the oviducts of control animals at 0900 h on Day 25. In the controls, PA activity in extracts of homogenized ovaries increased 3-fold from 0.125 +/- 0.010 OD units just before the administration of hCG to 0.371 +/- 0.021 at 12 h after hCG, i.e., near the time of ovulation. Indomethacin, in doses of 0.1-1.0 mg/rat, inhibited ovulation but did not inhibit the normal increase in PA activity, whereas indomethacin at the high dose of 10.0 mg/rat inhibited both ovulation and PA activity. Cycloheximide, at a dose of 0.1 mg/rat, was given at 12 h before hCG, immediately after hCG, and at 9 h after hCG. This agent inhibited ovulation most effectively when given at 12 h before hCG, yet it inhibited PA activity most effectively when given immediately after or at 9 h after hCG. Colchicine, at a dose of 0.1 mg/rat, inhibited ovulation, but not PA activity, when it was given 1 h before hCG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Structure-activity relationships of estrogens: effects of esterification of the 11 beta-hydroxyl group

Fourteen esters (formate, acetate, propionate, butyrate, hexanoate, heptanoate, and benzoate) located at C-11 of 11 beta-hydroxyesterone and 11 beta-hydroxyestradiol-17 beta were synthesized and evaluated for uterotropic and gonadotropin release inhibition in rats, as well as their ability to displace (3H) estradiol-17 beta from the rat uterine cytosolic estrogen receptor. The most potent uterotropic agent was 11 beta-formoxyestrone which was 1,625 or 2,500 times as active as 11 beta-hydroxyesterone in the uterotropic or gonadotropin release inhibition assay, respectively. 11 beta-Formoxyestrone was 7.5 times as uterotropic as estradiol-17 beta and equal to estradiol-17 beta in inhibiting gonadotropin release. However, the most potent inhibitor of gonadotropin release was 11 beta-acetoxy-estradiol-17 beta which had 133% of the activity of estradiol-17 beta, although it had only 38% of the activity of estradiol-17 beta in the uterotropic assay. Esters larger than the acetoxy group showed sharply decreased activities in either assay. Despite the high estrogenic potency of the 11-formates or 11-acetates, they were rather weak (6% to 35% as active as estradiol-17 beta) in displacing (3H) estradiol-17 beta from the rat uterine cytosolic estrogen receptor.     

Ovarian follicular wave synchronization and induction of ovulation in postpartum beef cows

An experiment was designed to evaluate a) the effect of a progesterone-estradiol combined treatment on ovarian follicular dynamics in postpartum beef cows, and b) ovulation and the subsequent luteal activity after short-term calf removal and GnRH agonist treatment. Multiparous Angus cows (25 to 40 d after calving) were assigned to the following treatments: untreated (Control, n = 9); short term calf removal (CR, n = 8); progesterone (CIDR, n = 9) and progesterone plus estradiol-17 beta (CIDR + E-17 beta, n = 9). Progesterone treatment (CIDR) lasted 8 d and the day of device insertion was considered as Day 0. Cows in the CIDR + E-17 beta group also received an i.m. injection of 5 mg of E-17 beta on Day 1. On Day 8, calves were removed for 48 h (CR, CIDR and CIDR + E-17 beta groups) and 6 h before the end of calf removal these cows also received an i.m. injection of 8 micrograms of Busereline (GnRH). Anestrus was confirmed in all cows by the absence of luteal tissue and progesterone concentrations below 1 ng ml-1 at the beginning of the experiment. Although mean (+/- SEM) interval from the beginning of the experiment (Day 0) to wave emergence did not differ (P > 0.05) among treatment groups (Control, 1.9 +/- 1.0, range -2 to 7 d; CR, 3.9 +/- 0.7, range 0 to 6 d; CIDR, 2.8 +/- 0.5, range 0 to 4 d and CIDR + E-17 beta, 4.1 +/- 0.2, range 3 to 5), the variability was less (P < 0.05) in the CIDR + E-17 beta group. The proportion of cows ovulating 24 to 48 h after GnRH administration tended (P = 0.08) to be higher in cows from CIDR + E-17 beta group (8/9) than in those of CR (5/8) or CIDR (6/9) groups, respectively and was associated with a higher proportion (P < 0.05) of CIDR + E-17 beta treated cows (9/9) that had a dominant follicle in the growing/early static phase at the time of GnRH treatment compared to the other GnRH treated groups (5/8, and 4/9 for CR and CIDR groups, respectively). Two CR cows ovulated 0-24 h after GnRH and only one Control cow ovulated the day before the time of GnRH administration. Cows pretreated with progesterone had longer (P < 0.05) luteal lifespan (CIDR, 14.5 +/- 0.7, CIDR + E-17 beta, 13.9 +/- 0.6 d) than those not treated with CIDR (Control, 5, CR, 4.0 +/- 0.4). We conclude that progesterone plus estradiol treatment results in tightly synchronized wave emergence and high GnRH-induced ovulation rate with normal luteal activity in postpartum beef cattle.     

Effects of indomethacin and aminoglutethimide phosphate in vivo on luteinizing-hormone-induced alterations of cyclic adenosine monophosphate, prostaglandin F, and steroid levels in preovulatory rat ovaries.

Changes in levels of cyclic adenosine monophosphate (cAMP), prostaglandin F (PGF), progesterone, testosterone, and estradiol-17beta, in preovulatory rat ovaries induced by exogenous luteinizing hormone (LH) have been measured. Ovarian cAMP reached maximal levels 15 min and 1h after LH administration by intravenous and intraperitoneal routes, respectively, and then declined to pre-LH levels by 8 h. Progesterone levels in ovaries and serum rose approximately in parallel with cAMP, but remained elevated throughout the 8-h sampling period. Ovarian testosterone increased to maximal levels 1 h after LH injection, followed by a rapid decline to below pre-LH levels. Ovarian estradiol-17beat concentrations declined steadily throughout the sampling period, reaching almost undetectable levels 8 h after LH treatment. Elevated ovarian PGF levels were observed only at the 4- and 8-h sampling times. Indomethacin treatment, 1 h before LH, prevented the LH-induced increase in ovarian PGF levels, depressed PGF values considerably in saline-injected controls but produced no significant inhibition of ovarian cAMP and progesterone levels. Aminoglutethimide phosphate depressed ovarian concentrations of all three steroids (progesterone, testosterone, and estradiol-17beta) to essentially undetectable levels, both in control and LH-injected rats, but did not alter the LH-induced changes in ovarian cAMP and PGF levels. These observations support the concept of cAMP as a mediator of the LH-induced alterations of ovarian steroidogenesis in vivo during the preovulatory period, but argue against an obligatory role of PGF in this process.     

Serum LH,progesterone and estradiol-17β levels throughout the ovarian cycle,during the early stage of pregnancy and after the parturition and the abortion in the common marmoset,Callithrix jacchus

In the ovarian cycle of common marmosets, serum progesterone began to increase at two to three days after estradiol-17β or LH surge, attained a peak of 25–70 ng/ml and then declined to a level of under 2 ng/ml before the ensuing rise in estradiol-17β and LH. Serum estradiol-17β increased to 700–5,500 pg/ml during the luteal phase, synchronizing with progesterone. It is suggested that the corpus luteum secreted estradiol-17β as well as progesterone. The cycle length as determined from the interval between successive LH surges was approximately 28 days. During the luteal phase, the levels of progesterone and estradiol-17β were higher than in Old World monkeys and women, but marmosets were not accompanied by any clinical symptoms due to excessive progesterone and estradiol-17β. This suggests that such unresponsiveness to progesterone and estradiol-17β in marmosets reflects the small amount of estradiol-17β receptor and presumably also the lower function of the post receptor system. Recovery of the post-partum ovarian cycle in two marmosets differed from that observed in Old World monkeys and women. The first LH surge was found on the ninth and tenth day after parturition and the first ovulation led to the next pregnancy. This suggests that the suckling stimulus of newborns in the common marmoset does not cause any delay in recovery of the ovarian cycle. In three cases of abortion, the recovery of the ovarian cycle was almost the same as that in the case of normal parturition: the first LH surge appeared on the 10th, 14th, and 34th day after abortion.     

Postpartum acyclicity in suckled beef cows: a review

Prolonged postpartum acyclicity in suckled beef cows is a source of economic loss to beef cattle producers. Duration of postpartum acyclicity is influenced by suckling status, nutritional status, calving season, age, and several other factors. Although uterine involution begins and ovarian follicular waves resume soon after parturition, dominant follicles of these waves fail to ovulate, due to a failure to undergo terminal maturation. As a result, postpartum anovulatory dominant follicles are smaller than the ovulatory follicles in cyclic cows. Failure of postpartum dominant follicles to undergo terminal maturation is due to absence of appropriate LH pulses, a prerequisite for follicular terminal maturation prior to ovulation. Absence of LH pulses early post partum is primarily due to depletion of anterior pituitary LH stores, although GnRH pulses are also absent during this period due to suckling. Following replenishment of LH stores between Days 15 and 30 post partum, absence of LH pulses is due to continued sensitivity of the hypothalamic GnRH pulse-generator to the negative feedback effect of ovarian estradiol-17beta, which results in absence of GnRH pulses. This negative feedback effect of estradiol-17beta is modulated by suckling which stimulates release of endogenous opioid peptides from the hypothalamus. As the postpartum interval increases, sensitivity of the GnRH pulse-generator to the negative feedback effect of ovarian estradiol-17beta decreases. This is followed by an increasing frequency of GnRH discharges and LH pulses, terminal follicular maturation, ovulation, and continued cyclicity. The first ovulation post partum is usually followed by a short cycle due to premature luteolysis because of premature release of PGF2alpha from the uterine endometrium, which is possibly intensified by the suckling-induced oxytocin release from the posterior pituitary. A model for the postpartum ovulatory acyclicity and for the resumption of cyclicity is presented.     

Effects of luteinizing hormone and follicle-stimulating hormone and insulin-like growth factor-I on aromatase activity and P450 aromatase gene expression in the ovarian follicles of red seabream,Pagrus major

To clarify the mechanism of estradiol-17beta production in the ovarian follicle of red seabream, in vitro effects of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and insulin-like growth factor (IGF-I) on aromatase activity (conversion of testosterone to estradiol-17beta) and cytochrome P450 aromatase (P450arom) mRNA expression in ovarian fragments of red seabream were investigated. Of the growth factors used in the present study, only IGF-I stimulated both aromatase activity and P450arom gene expression in the ovarian fragments of red seabream. LH from red seabream pituitary, but not FSH, stimulated both aromatase activity and P450arom gene expression. IGF-I slightly enhanced the LH-induced aromatase activity and P450arom gene expression. These data and our previous results indicate that LH, but not FSH, stimulates estradiol-17beta production in the ovarian follicle of red seabream through stimulation of aromatase activity and P450arom gene expression and IGF-I enhances the LH-stimulated P450arom gene expression.     

Oviductal isthmic motility in relation to ovulation and endocrine changes in unrestrained sows

This study was designed to characterize changes in the motility of the oviductal isthmus in relation to endocrine changes around ovulation in unrestrained sows in their normal environment. Oviductal isthmic motility was monitored on Polyview from 11 h prior to and up to 36 h after ovulation in 13 unrestrained multiparous sows during their second estrus after weaning, using a pressure microtransducer implanted 3 cm into the isthmus. Both the maximum, minimum and mean pressures and the frequency of phasic pressure fluctuations were high prior to ovulation but declined significantly (P<0.05) at 9 to 12 h, 13 to 16 h, 13 to 16 h and 5 to 8 h after ovulation, respectively. Plasma estradiol-17beta and prostaglandin F2alpha metabolite levels declined significantly (P<0.05) at 4 to 7 h prior to ovulation while progesterone levels increased significantly (P<0.01) at 5 to 8 h after ovulation. The decrease in the plasma estradiol-17beta levels was correlated to the decrease in maximum and mean pressures and the frequency of phasic pressure fluctuations (n=113; r=0.30, 0.25, 0.25, respectively; P<0.01) but not to the decrease in minimum pressure (n=113; r=0.17, P>0.05). Similarly, the decrease in PGF2alpha metabolite levels was correlated to the decrease in minimum, maximum and mean pressures and the frequency of phasic pressure fluctuations (n=112; r=0.43, 0.35, 0.38, 0.32, respectively; P<0.001). Conversely, the increase in plasma progesterone levels was correlated to the decrease in minimum, maximum and mean pressures and the frequency of phasic pressure fluctuations (n=113; r=-0.56, -0.70, -0.68, -0.60, respectively; P<0.001). Therefore, the pressure parameters seem to be influenced by changes in the levels of estradiol-17beta, prostaglandin F2alpha and progesterone with respect to ovulation.     

Uterine involution, day and variance of first postpartum ovulation in mares treated with progesterone and estradiol-17beta for 1 or 2 days postpartum

The effects of a single or double regimen of exogenous progesterone and estradiol-17beta (P/E, total dose 300 mg P/20 mg E) were investigated in 50 postparturient Quarter Horse mares. In Trial 1, at 1 and 24 h after foaling, mares were injected with progesterone (150 mg) and estradiol-17beta (10 mg) (n = 7) or 0.9% NaCl (control, n = 13). In Trial 2, within 12 h after foaling, mares were injected with progesterone (300 mg) and estradiol-17beta (20 mg) (n = 13) or 0.9% NaCl (control, n = 17). Mares were examined daily by palpation per rectum and transrectal ultrasonography to determine the day of ovulation. The largest cross sectional diameters of each uterine horn and uterine body were measured ultrasonographically on Day 15 postpartum. Mean uterine diameters did not differ between treatment groups (P > 0.05) in Trial 1, Trial 2 or for combined data for both Trials 1 and 2. For mares bred on the first postpartum estrus pregnancy rates did not differ (P > 0.05) between treatment groups (16/18, 89%) and controls (22/30, 81%) nor was there a difference in mean day to first postpartum ovulation (P > 0.05) between treated and control groups in Trial 1, Trial 2 or Trials 1 and 2 combined. However, fewer (P < 0.05) total P/E treated mares (0/20) ovulated prior to Day 10 postpartum than did control mares (6/30). Variance in days to ovulation was lower (P < 0.05) for P/E treated mares (var = 3.73 days) than for control mares (var = 7.64 days) for data combined from Trials 1 and 2.     

Effect of progestogen plus estradiol-17beta treatment on superovulatory response in beef cattle

A series of 3 experiments were conducted to evaluate superovulatory response following exogenously controlled follicular wave emergence in cattle. In Experiment 1 the hypothesis was tested that treatments with progestogen plus estradiol-17beta (E-17beta) would result in the emergence of a wave of ovarian follicles that are as responsive to exogenous gonadotropins as those of a spontaneous follicular wave. Beef cows and heifers either received a progestogen ear implant on Day 0 (ovulation) plus 5 mg im E-17beta on Day 1 and were superstimulated on Day 5, or did not receive implants but were superstimulated on Day 8 (expected day of emergence of the second follicular wave). The cattle received 400 mg NIH-FSH-P1 of Folltropin-V, given in a single subcutaneous injection or twice daily as intramuscular injections over 4 d. No significant differences were detected between the 2 groups in the number of corpora lutea (CL), ova/embryos collected, fertilized ova and transferable embryos. In Experiment 2 superstimulatory responses to a single subcutaneous injection of Folltropin-V were compared between heifers in which follicle wave emergence was synchronized with progestogen plus E-17beta at unknown stages of the estrous cycle with those treated following a conventional method of superstimulation at middiestrus. Superstimulation 4 d after E-17beta treatment in heifers with progestogen implants resulted in a similar superovulatory response and higher fertilization rates than those initiated 8 to 12 d after estrus. In Experiment 3 the ovarian response to a single- versus multiple-injection superstimulatory treatment protocol was compared in heifers given progestogen plus E-17beta to induce synchronous wave emergence. The number of CL, ova/embryos collected, fertilized ova and viable embryos were not different between groups. Superstimulatory treatments initiated 4 d after E-17beta treatment of cattle with progestogen implants resulted in comparable ovulatory responses to treatments initiated at the time of spontaneous wave emergence or during middiestrus. Synchronizing wave emergence in a group of randomly cycling cattle obviated the need of estrus detection and synchronization prior to superstimulation.     

Regulation of follicle-stimulating hormone secretion by estradiol and dimeric inhibins in the infantile female rat.

Plasma and ovarian levels of the dimeric forms of inhibin and plasma estradiol-17beta were investigated and compared with changes in plasma gonadotropins from Postnatal Day (PND) 5 to PND 30 in the female rat. The inhibin subunit proteins were localized in follicular granulosa cells of the ovary. Plasma immunoreactive inhibin levels were low until PND 15 and increased thereafter. Plasma levels of inhibin B (alpha and beta(B) subunits) remained very low until PND 15 and then increased by approximately 24-fold. In contrast, plasma levels of inhibin A (alpha and beta(A) subunits) were relatively low and steady until PND 20, then increased by approximately 3-fold at PND 25. Changes in ovarian inhibin A and B levels closely resembled those in plasma levels. Plasma FSH levels were low at PND 10 but started to peak from PND 15 and remained high until PND 20, followed by a remarkable reduction at PNDs 25 and 30. This dramatic fall in FSH coincided with the rise of inhibin A. A significant inverse correlation was observed between plasma FSH and plasma inhibin A (r = -0.67, P < 0.0002), ovarian inhibin A (r = -0.48, P < 0.01), plasma inhibin B (r = -0.48, P < 0.05), and ovarian inhibin B (r = -0.54, P < 0.01). Plasma estradiol-17beta levels were elevated from PND 5 through PND 15, then fell sharply through PND 30. Plasma estradiol-17beta was significantly and positively (r = 0.75, P < 0.0002) correlated with plasma FSH. Plasma LH rose to higher levels at PND 15 and tended to be lower thereafter. The inhibin alpha, beta(A), and beta(B) subunits were localized to primary, secondary, and antral and large antral follicles, but the types of these immunopositive follicles varied with age. It appeared that, at PND 25 and afterward, all three subunits were mainly confined to large antral follicles in the ovary. We conclude that estradiol-17beta likely is the major candidate in stimulation of FSH secretion in the infantile female rat. We also conclude that inhibin regulation of pituitary FSH secretion through its negative feedback in the infantile female rat begins to operate after PND 20. We suggest that this negative feedback is achieved by increases in plasma levels of the two dimeric forms, and that inhibin A appears to be the major physiological regulator of FSH secretion at the initiation of this mechanism. We also conclude that large antral follicles in the ovary are the primary source of these bioactive inhibins that are secreted in large amounts into the circulation after PND 20.