Rise In Luteinizing Hormone Research Articles

Effects of preoptic injections of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide and PHI on the secretion of luteinizing hormone and prolactin in ovariectomized estrogen-primed rats

The effects of intracerebral injections of brain-gut peptides in the preoptic region on the secretion of luteinizing hormone (LH) and prolactin (PRL) were examined in ovariectomized, estrogen-primed rats. Gastrin or cholecystokinin-octapeptide injection in the preoptic region induced a moderate increase of circadian rise of LH secretion in some animals but no appreciable change in PRL secretion. Secretin injection was strikingly effective in increasing circadian rise of LH and PRL secretion. Vasoactive intestinal peptide injection completely abolished the occurrence of circadian rise of LH secretion whereas PHI injection facilitated LH secretion undergoing the circadian rhythm. The results suggest that those peptides act as neurotransmitters or neuromodulators in the preoptic region and are implicated in the regulation of LH and PRL secretion.

Plasma reproductive hormones in normal and vasectomized Chinese males.

Plasma reproductive hormones (testosterone, LH, FSH and prolactin) were measured in 298 normal healthy males aged 30-73 years from rural areas of Sichuan Province, People's Republic of China, and in 505 similar men vasectomized between 1 year and 25 years previously. Age-related increases in LH and FSH but not in testosterone or prolactin were noted in normal men. No adverse effects of vasectomy were observed apart from a 16% increase in mean LH levels in the vasectomized compared to non-vasectomized men of similar ages.

Dopaminergic regulation of gonadotropin levels and pulsatility in normal women

This study was done to define the concentration of dopamine (DA) that inhibits gonadotropin secretion and to study the effect of DA D-2 receptor blockade during the infusions. Normal women received 5-hour infusions of either glucose (n = 14) or DA at rates of 0.04 (n = 6), 0.4 (n = 6), and 4.0 micrograms/kg X minute (n = 9). After 3 hours, metoclopramide (MTC) was administered. Mean serum luteinizing hormone (LH) concentration declined during 0.4 (P less than 0.01) and 4.0 micrograms/kg X minute (P less than 0.05) infusion doses of DA. This effect of DA was not consistently (P greater than 0.05) antagonized by MTC. Six women received DA (4.0 micrograms/kg X minute) or glucose for 18 hours. After 17 hours, MTC was given. Blood samples were collected every 10 minutes during the last 8 hours. No significant effect on LH pulse frequency and pulse amplitude was observed (P greater than 0.05). A marked (P less than 0.01) rise in LH occurred after MTC administration. The authors conclude that (1) physiologic doses of DA may inhibit LH secretion with only little, if any, effect on the pulsatile release; and (2) low-affinity DA receptors responsive to DA D-2 antagonists may regulate LH secretion.

Relationships between luteinizing hormone, follicle-stimulating hormone and prolactin secretion and ovarian follicular development in the weaned sow.

Folliculogenesis was studied by assessing development of the largest 10 follicles obtained from 10 sows 48 h after weaning and by analyzing changes in plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) for 24 h before weaning until 48 h after weaning. Follicular diameter, follicular fluid volume, and concentrations of estradiol and testosterone and granulosa cell numbers were determined in all follicles, and 125I-hCG binding to theca and granulosa and maximal aromatase activity in vitro was determined in five follicles/sow. Overall, a significant rise in LH, but not in FSH, occurred at weaning, although in individual sows an increase in LH was not necessarily related to subsequent estrogenic activity of follicles. In 9/10 sows, PRL fell precipitously after weaning. In lactation, LH was negatively, and after weaning, positively, correlated with FSH and PRL. Marked variability in follicular development existed within and between sows. Overall, most follicular characteristics were positively correlated to follicular diameter; however, in larger follicles the number of granulosa cells was variable and unrelated to estrogenic activity, which--together with theca and granulosa binding of hCG--increased abruptly at particular stages of follicular development. Differences in maturation of similarly sized follicles from different sows were related to estrogenic activity of the dominant follicles but not to consistent differences in LH, FSH or PRL secretion. Both the dynamics and the control of folliculogenesis in the sow, therefore, appear to be complex.

Effects of preoptic microinjection of neurotensin on luteinizing hormone secretion in unanesthetized ovariectomized rats with or without estrogen priming.

Effects of microinjection of neurotensin (NT) in the medial preoptic area on luteinizing hormone (LH) release were examined in unanesthetized ovariectomized rats with or without estrogen priming. Microinjection of NT (100 ng) into the medial preoptic area of ovariectomized estrogen-primed rats significantly facilitated the circadian afternoon rise of LH secretion as compared to the hormone values in control animals microinjected with physiological saline. The timing of the afternoon LH rise was not altered by the peptide. In ovariectomized estrogen-unprimed rats, on the other hand, NT did not affect the existing pulsatile LH secretion nor induced an afternoon rise of the hormone secretion. These results show that NT can stimulate the preoptic LH release mechanism which undergoes the circadian clock under the influence of estrogen.

Kainic acid lesioning of the preoptic area alters positive feedback of estrogen in prepubertal female rats.

Stereotaxic infusion of kainic acid (KA) was performed to induce intrinsic neural lesions of the preoptic area (POA) in 25-day-old female rats. After KA infusion, rats in Experiment 1 received 10 micrograms of estradiol benzoate (EB) administered subcutaneously to assess positive feedback of EB on release of luteinizing hormone (LH) from the pituitary gland. Rats were perfused for light microscopic (LM) or electron microscopic (EM) evaluation of the lesion site. Rats of Experiment 2 were allowed to develop until the appearance of vaginal opening (VO) after which time vaginal lavages were taken to monitor the cyclicity of the vaginal epithelium. At 50 days of age, the right ovary from each rat was removed, trimmed of fat, and weighed. At 60 days of age, the remaining ovary was removed to assess compensatory ovarian hypertrophy (COH). In Experiment 3, we investigated the effects of POA/KA-infusion on sexual behavior. Sex behavior tests were conducted at 48 h after EB during the dark phase of the light cycle. In Experiment 1, all the control and saline-infused rats exhibited the expected rise of plasma LH two days after estrogen injection while the POA/KA-infusion abolished the positive feedback effect of EB on LH release. Ultrastructural examination of the lesion site revealed that neurons were undergoing acute degeneration while axons and afferent terminals seen in the same fields of analysis were morphologically intact. Preoptic area/KA lesions caused a marked delay in the appearance of VO. Duration of this temporal delay in POA/KA-lesioned rats was approximately 4 days, or one vaginal cycle. The lesioned animals showed normal compensatory hypertrophy after unilateral ovariectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Subtle abnormalities in follicular development and hormonal profile in women with unexplained infertility

A prospective study of six unselected couples diagnosed as having unexplained infertility was done. In three of six patients, subtle abnormalities in follicular development were detected. In the first case poor follicular growth was observed. There was a premature small rise of luteinizing hormone (LH) with subsequent low levels of estradiol (E 2 ) in the late follicular phase and unusual wide LH peak. This was followed by low progesterone levels in the luteal phase. In the second case follicular growth was abrupted by premature LH surge. This surge was triggered by early rise of E 2 level while the follicle was still small in size. In the third case luteinized unruptured follicle syndrome was diagnosed, on ultrasound examination. All of the abnormalities were repetitive.

Changes in Circulating Levels of Immunoreactive Follicle Stimulating Hormone, Luteinizing Hormone, and Testosterone During Sexual Development in the Rhesus Monkey, Macaca mulatta

Basal serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) and the responsiveness of these hormones to a challenge dose of luteinizing hormone releasing hormone (LHRH), were determined in juvenile, pubertal, and adult rhesus monkeys. The monkey gonadotrophins were analyzed using RIA reagents supplied by the World Health Organization (WHO) Special Programme of Human Reproduction. The FSH levels which were near the assay sensitivity in immature monkeys (2.4 +/- 0.8 ng/ml) showed a discernible increase in pubertal animals (6.4 +/- 1.8 ng/ml). Compared to other two age groups, the serum FSH concentration was markedly higher (16.1 +/- 1.8 ng/ml) in adults. Serum LH levels were below the detectable limits of the assay in juvenile monkeys but rose to 16.2 +/- 3.1 ng/ml in pubertal animals. When compared to pubertal animals, a two-fold increase in LH levels paralleled changes in serum LH during the three developmental stages. Response of serum gonadotrophins and T levels to a challenge dose of LHRH (2.5 micrograms; i.v.) was variable in the different age groups. The present data suggest: an asynchronous rise of FSH and LH during the pubertal period and a temporal correlation between the testicular size and FSH concentrations; the challenge dose of LHRH, which induces a significant rise in serum LH and T levels, fails to elicit an FSH response in all the three age groups; and the pubertal as compared to adult monkeys release significantly larger quantities of LH in response to exogenous LHRH.

Reproductive physiology of the clouded leopard: II. A circannual analysis of adrenal-pituitary-testicular relationships during electroejaculation or after an adrenocorticotropin hormone challenge.

A circannual analysis was made of serum cortisol, luteinizing hormone (LH), and testosterone concentrations in the male clouded leopard (Neofelis nebulosa). Group I males (n = 4), maintained in a standardized environment, were bled serially during a regimented anesthesia/electroejaculation episode occurring monthly (beginning in January, ending in December). Additional sampling intervals were conducted under anesthesia only (control, n = 8), anesthesia plus a single adrenocorticotropin hormone challenge (ACTH, Cortrosyn, n = 4), or anesthesia plus a single 25 micrograms injection of gonadotropin-releasing hormone (GnRH, Gonadorelin, n = 4). Group II males (n = 6) from various zoological collections were sampled serially under the same semen collection conditions on one random occasion within the year. Serum cortisol levels were 2 times greater than values measured in comparable studies involving other felid species. Cortisol concentrations were similar during electroejaculation and control (anesthesia only) episodes, and mean levels did not rise as a result of semen collection. Adrenocorticotropin caused an immediate rise in cortisol to levels at least 1.5 times greater than electroejaculated or control counterparts. Mean concentrations of basal cortisol in individual males gradually increased as the year progressed, possibly as a consequence of repeated psychogenic stress. Between seasons, there were no differences in mean LH; however, testosterone levels were greater (p less than 0.05) in the winter compared to all other seasons. There were no differences (p greater than 0.05) between individual males in secretory patterns or mean concentrations of cortisol, LH, or testosterone. Within males, distinct temporal fluctuations were observed in both LH and testosterone during the approximately 80-min sampling interval. Neither LH nor testosterone profiles appeared affected by cortisol patterns during electroejaculation or after an ACTH challenge. A bolus of GnRH induced a marked rise in serum LH and testosterone within 15 and 30 min respectively, indicating that these two hormones were coupled. Both LH and testosterone profiles in Group II males mimicked those in Group I; concentrations of cortisol in Group II males immobilized on one occasion were similar to those of Group I animals sampled from January-May but appeared to be less than values measured from June-December. These data demonstrate that the clouded leopard, compared to other felids, produces markedly elevated concentrations of cortisol, which are likely related to an aggressive behavioral temperament.(ABSTRACT TRUNCATED AT 400 WORDS)

In vitro fertilization and embryo transfer as related to endogenous luteinizing hormone rise or human chorionic gonadotropin administration

After ovarian stimulation with clomiphene citrate combined with human menopausal gonadotropin for in vitro fertilization, the appearance of a spontaneous luteinizing hormone (LH) surge before fulfillment of the minimal criteria of follicular maturity (at least one follicle greater than 19 mm and serum estradiol [E2] greater than 400 pg/ml/follicle greater than 17 mm) is associated with reduced pregnancy rates. In these cases, follicles are smaller and serum E2 values are lower at the time of the LH surge. Oocyte recovery rate is reduced, embryonic anucleate fragments are more frequently observed, and the level of luteal progesterone on day 4 after oocyte retrieval is lower. Hyperandrogenic patients are more prone to display such premature spontaneous LH surge. We concluded that in case of an untimely LH rise, laparoscopy for oocyte retrieval should be cancelled.

Gonadotropin responses to naloxone may depend upon spontaneous activity in noradrenergic neurons at the time of treatment

The opiate system is thought to modulate gonadotropin secretion by its effect on catecholamine secretion. This action may be produced by opiates regulating the amount of catecholamine released from presynaptic terminals at a given frequency of depolarization and/or by increasing the rate of impulse traffic within catecholamine neurons. We examined the effects of naloxone, an opiate receptor antagonist, on luteinizing hormone (LH) and prolactin (Prl) secretion in 3 sex steroid-treated, gonadectomized rat models in which we have considerable information on the rates of turnover of norepinephrine (NE) and dopamine (DA) in the hypothalamus. In 7 day ovariectomized rats treated for 2 days with estradiol (E 2), the injection of naloxone (10 mg/kg) at 09.15 h produced a small 3-fold rise in LH and a short-lived decline in Prl. In contrast, naloxone, given at 12.15 h, markedly amplified (10-fold) and advanced the time of the LH surge but did not affect afternoon Prl surges. Hypothalamic NE turnovers are low in the morning and high in the afternoon for such animals. Other ovariectomized (OVX) rats received E 2 for 2 days and progesterone (P 4) on day 2. Such treatment extinguishes the LH surges which normally occur the next day (day 3) but does not affect phasic Prl secretion. Naloxone, given at 09.15 h to E 2P 4-treated rats on day 3, did not affect basal LH levels but serum Prl declined for about 1 h. When given at 12.15 h, naloxone produced a small 3-fold rise in LH but did not affect phasic Prl release. E 2P 4-treated OVX rats do not show increases in hypothalamic NE turnover during the afternoon and have a rate high of DA turnover in the median eminence. The final group of rats were 7 day castrated males treated for 2 days with E 2. Such rats do not display LH or Prl surges in response to E 2 and catechol turnovers are not different between morning and afternoon. Naloxone, given at 09.00 h, produced a small, rapid, 2.5-fold rise in LH and a decline in Prl within 15 min but basal levels were reestablished by 10.00 h. An almost identical response occurred when naloxone was given at 12.15 h. These data, when considered together with previously published information from this laboratory on hypothalamic catecholamine turnover rates, suggest that when hypothalamic NE turnover is low only small rises in LH occur compared to magnified LH responses obtained in animals which have high rates of NE turnover. Seemingly, these effects are mediated primarily at presynaptic NE terminals to permit the more efficient release of NE rather than by increasing the frequency at which catechol neurons depolarize. Further, the observation that naloxone does not affect phasic Prl release in steroid-treated females suggests that catecholamines are not the principle neurotransmitters regulating phasic Prl release.

Changes in plasma concentrations of luteinizing hormone, progesterone and oestradiol-17β during the periovulatory period in cyclic swamp buffaloes ( Bubalus bubalis)

Changes in plasma concentrations of luteinizing hormone (LH), progesterone and oestradiol-17β were analysed in relation to the chronology of behavioural oestrus and ovulation in six cyclic swamp buffaloes. Blood samples were collected every 3–6 h from Day 17 of the cycle until ovulation, with additional samples for LH determination only taken at 1-h intervals during oestrus. The time of oestrus manifestation and ovulation was checked every 3 h throughout the experiments by using a vasectomized bull or by rectal palpation, respectively. Animals came in oestrus between Days 19 and 22, with a mean duration of oestrus of 20.5 ± 1.2 h (± s.e.m.). Ovulation was detected at 15 to 18 h after the end of oestrus. Plasma concentrations of progesterone began to decrease 2–3 days before oestrus manifestation. The progesterone withdrawal during luteolysis was followed by a threefold rise ( P < 0.05) in the basal LH and a sustained increase ( P < 0.05) in oestradiol concentrations. Oestradiol levels reached maximum values near the onset of oestrus and rapidly decreased to the basal levels by the end of oestrus. LH surge began immediately after the onset of oestrus and lasted 7–12 h. The LH peak (61–126 ng/ml) was observed 4–15 h after the onset of oestrus or 9–14 h before the end of oestrus. Ovulation occurred within a fixed time of 26–29 h after the LH peak. The data obtained here were basically similar to those well documented in cattle, although the cause and effect relationship between each endocrine event still requires further clarification.

Roles of pattern of secretion of luteinizing hormone and the ovary in attainment of puberty in ewes lambs

Four experiments were conducted to examine (1) how patterns of luteinizing hormone (LH) change as lambs approach first estrus, (2) whether mimicry of these changes by exogenous LH will initiate events of the pubertal process, (3) aspects of possible roles of the ovary and estradiol in the initiation of an ovulatory surge of LH in prepubertal lambs and (4) the time requirements for the presence of the ovary in induction of that surge of LH. In 19 lambs (Exp. 1), concentrations of LH in plasma were higher at puberty than 7 weeks earlier. Increased concentrations of LH in samples taken every 20 min for 6 hr during the luteal and follicular phases preceding first estrus were attributed to increased amplitude, but not increased frequency, of episodic pulses of LH. In Exp. 2, endocrine events which are included in the natural onset of ovarian cyclic activity (i.e. surge of LH and subsequent rise in progesterone) were initiated in 5 6 , 4 6 , 1 5 , 1 6 , and 3 6 lambs, receiving either injections of 7.5 μg/hr, 15 μg/hr, 30 μg/2hr, 45 μg/3hr or constant infusions of 15 μg/hr of purified ovine LH, respectively. However, these lambs did not exhibit estrus or cyclic ovarian activity. In Exp. 3, the mechanism by which hourly injections of LH prompted surges of LH was determined to be mediated through ovarian stimulation and not through a direct effect of exogenous LH on the hypothalamo-pituitary axis. All the intact (n=5) but no acutely (two weeks) ovariectomized (n=5) lambs had a preovulatory-like surge in response to exogenous LH. Further, (Exp. 4) it was shown that the ovarian signal must be maintained or evoked within 6 hr preceding the surge of LH, because lambs (n=20) ovariectomized at or 9, 18 or 27 hr after initiation of the exogenous LH with the one exception failed to show a surge of LH. It could not be demonstrated that the ovarian signal involved changes in peripheral concentrations of androstenedione, testosterone or estradiol-17β, although patterns of LH in ovariectomized lambs were responsive to both negative and positive feedback effects of estradiol (n=6, Exp. 3) and in general estradiol levels were increasing prior to the induced surge of LH.

Evidence for a positive feedback interaction between progesterone and luteinizing hormone in the induction of ovulation in the hen, Gallus domesticus

Two experiments were conducted to test the hypothesis that progesterone (P 4) acts to induce a preovulatory rise of luteinizing hormone (LH) by initiating a true positive feedback interaction between P 4 and LH. In each experiment, ten hens were stereotaxically implanted with a third ventricle cannula. Aminoglutethimide phosphate (AGP), an inhibitor of steroidogenesis, was administered (200 mg iv) to hens at 10 and 6 hr (Experiment 1) and 10 and 7 hr (Experiment 2) before an expected C 1 ovulation. A 20-μg injection of P 4 ( n = 5) or the vehicle ( n = 5) was made intraventricularly at 6 hr (Experiment 1) or 7 hr (Experiment 2) before the expected ovulation. Blood samples were taken via branchial vein cannula at regular intervals after the injection. In Experiment 1, four of five P 4-treated hens ovulated, and no atretic follicles were found in any of the five P 4-treated hens, including the one which did not ovulate. Ovulations were always accompanied by preovulatory LH peaks. By comparison, none of the vehicle-injected animals ovulated and in four of five hens the largest follicle was determined to be atretic. No ovulations occurred in Experiment 2 for either the P 4- or vehicle-injected hens. Atresia of the largest follicle occurred in all five hens in the P 4-treated group and four of five hens of the vehicle-treated group. The difference in results between Experiment 1 and Experiment 2 can be explained assuming that the steroidogenesis-inhibiting action of the initial AGP injection in Experiment 1 (at 10 hr before ovulation) had diminished prior to the second AGP treatment (at 6 h before ovulation). In both Experiments 1 and 2, intraventricular P 4 injection caused a significant ( P < 0.001 for Experiment 1; P < 0.03 for Experiment 2) rise in plasma P 4 within 10 min after injection due to leakage of P 4 from the third ventricle into the systemic circulation. Nevertheless, in the absence of any steroid feedback from the ovary (Experiment 2), the small rise in LH induced by the P 4 injection was not potentiated, and no preovulatory surge of LH occurred. These results support the hypothesis that a positive feedback interaction between P 4 and LH, in contrast to a stimulatory effect of P 4, is necessary for the preovulatory LH surge and ovulation.

Pituitary Gonadotropin-Independent Male-Limited Autosomal Dominant Sexual Precocity in Nine Generations: Familial Testotoxicosis

A recently described, distinct form of male sexual precocity is characterized by premature Leydig and germinal cell maturation in the absence of pituitary gonadotropin stimulation. Analysis of a nine-generation kidred with at least 28 affected males supports sex-limited autosomal dominant transmission. Three boys, with precocious sexual development at 1 to 4 years of age, had low basal plasma gonadotropin values without pubertal-type pulsatility and a minimal rise in luteinizing hormone after acute stimulation with luteinizing hormone releasing factor or its potent analog D-Trp 6 -Pro 9 -NEt-LRF, distinguishing them from boys with true precocious puberty. Two affected adults had a mature luteinizing hormone response to LRF. Testicular biopsies showed a progression of abnormalities in the seminiferous tubules from childhood to maturity; in one adult this disorder was associated with marked oligospermia and selective elevation of plasma follicle-stimulating hormone. The findings are consistent with an inherited intratesticular defect. Furthermore, the majority of cases of familial male sexual precocity seem to be examples of this disorder rather than central or true precocious puberty.

Coital stimuli controlling luteinizing hormone secretion and ovulation in the female ferret.

A series of experiments focused on the masculine coital behaviors controlling pituitary luteinizing hormone (LH) secretion and reflex ovulation in the estrous female ferret. An initial experiment investigated which coital stimuli from the male are required to induce ovulation. It was found that corpus luteum formation, which served as an index of ovulation, occurred in estrous female ferrets only if the male achieved a penile intromission. Neck gripping, mounting, and pelvic thrusting behavior without intromission by the male failed to induce ovulation. A second experiment investigated the timing and magnitude of the coitus-induced LH surge associated with ovulation. Blood was obtained via jugular catheters from estrous females in various mating situations. Plasma LH concentrations were measured by a heterologous radioimmunoassay that was validated for use in the ferret. A significant surge in plasma LH occurred only when an intromission was achieved by the stud male. Plasma LH was significantly elevated 2.0 h after the introduction of the male, peak values were reached 6.0 h later, and this elevation lasted on average 5.7 hours (5/5 females). No LH rise occurred in 2/2 female ferrets in which only neck gripping, mounting, and pelvic thrusting, but no intromission, were allowed to occur. The ferret mating pattern and the resultant LH response differ from those seen in three other induced ovulators (cat, vole, and rabbit) in which the male's intromission latency and duration are much shorter than in the ferret, and in which a distinctive peak in plasma LH often occurs within 1 h after mating.

Effect of suckling on the hypothalamic-pituitary axis in postpartum beef cows, independent of ovarian secretions.

Thirty-two postpartum (PP) cows were used to investigate the effect of suckling on secretion of luteinizing hormone (LH). Calves remained with their dams (suckled; S), or they were removed within 24 h of birth (nonsuckled; NS). To evaluate the relationship between suckling and negative feedback regulation of LH, cows were ovariectomized on Day 5 PP, then injected intravenously with estradiol-17 beta (E) or vehicle (V) on Day 10 PP. To investigate the influence of suckling on the gonadotropin-releasing hormone (GnRH)-induced release of LH, cows were injected with 80 micrograms of GnRH on a single day varying from 18 to 85 days PP. Suckling inhibited the postcastration rise in LH, as LH concentrations increased at a faster rate in NS compared with S cows [0.031 +/- 0.02 ng/(ml X day) LH: P less than 0.05]; this was not influenced by basal amounts of E since amounts did not differ between S and NS cows at ovariectomy (5.37 +/- 0.36 vs. 5.34 +/- 0.48 pg/ml E; P greater than 0.05). Serum concentrations of LH were negatively related to total follicular E only in S cows (r = -0.71; P less than 0.01). Estradiol-17 beta caused a decrease not only in the level but also the variability in LH concentrations in both S and NS cows: LH in S cows was less variable after E than in NS cows (P less than 0.001), but the magnitude of LH suppression was not influenced by suckling (P greater than 0.25). The regression of LH response on days PP was essentially the same over time for both S (P greater than 0.25) and NS (P greater than 0.25) cows, indicating that LH response to a GnRH injection was not influenced by suckling or days PP. Suckled cows had a tendency to release more LH relative to their baseline in response to GnRH as time PP increased (P less than 0.10), but NS cows did not. These results indicate that even though ovarian secretions inhibit LH release from the pituitary, other inhibitory influences may have a major effect in S cows. Concentrations of LH were lower in S cows than NS cows on Day 10 PP, following removal of the ovaries on Day 5, suggesting that suckling had a direct effect on the hypothalamic-pituitary axis.

Proestrous hormonal changes preceding the onset of ovulatory failure in lightly androgenized female rats.

Proestrous hormonal profiles were characterized in lightly androgenized female rats prior to the onset of the delayed anovulatory syndrome (DAS). In these females, ovulatory failure and persistent vaginal estrus (PVE) occur at a very early age. Female Sprague-Dawley rats were injected with 10 micrograms testosterone propionate (TP) on postnatal Day 5. Control rats were untreated. All animals were weaned at 21 days of age, and following the onset of puberty, estrous cyclicity was monitored by vaginal smear. Rats showing regular 4-day cycles were used. Between 50-70 days of age, intra-atrial cannulae were implanted on a morning of proestrus (0700-0900 h) and blood was sampled at 2-h intervals from 1000 to 2000 h. Additional samples were taken at 0.5-h intervals from 1600 to 1800 h. Plasma was assayed for luteinizing hormone (LH), follicle-stimulating hormone (FSH) and progesterone (P) by radioimmunoassay (RIA). All animals were monitored for the onset of PVE or other alterations in estrous cyclicity. Females treated neonatally with TP that subsequently showed PVE by 150 days of age (PRE DAS) displayed a reduced peak amplitude (P less than 0.01) and delay in onset (1600 vs. 1400 h) of LH but not FSH secretion, when compared to controls. Females treated neonatally with TP that did not enter PVE by 150 days of age (No DAS) also showed a delayed rise in LH when compared to controls. However, the amplitude of LH secretion was not different from controls or PRE DAS females.(ABSTRACT TRUNCATED AT 250 WORDS)

A comprehensive dose-response study of clomiphene citrate for enhancement of the primate ovarian/menstrual cycle

Despite the increasing use of clomiphene citrate (CC) in normally cycling women undergoing in vitro fertilization, comprehensive data on the dose-response effects of the drug are unavailable. Twenty-four adult, normally cycling monkeys were given CC on cycle days 5 through 9 in doses ranging from 1 mg/kg to 10 mg/kg. Serum estradiol (E2), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and progesterone were measured daily. CC stimulated an early, attenuated rise in serum LH which correlated with subsequent follicle development. Concurrently, serum E2 rose to preovulatory levels. No significant increase in serum FSH concentration was seen as a result of CC therapy. No correlation was seen between CC dose and peak levels of E2, LH, or FSH. The ovulatory status of the treatment cycles was also independent of dose. The factors that modulate these hormonal changes may involve direct effects of CC, estrogen feedback, and/or ovarian factors as yet uncharacterized. The individual variation of ovarian response, however, appears to be independent of the dose of CC.

Modulation of pulsatile luteinizing hormone secretion by ovarian steroids in the rat.

In this study, we have examined the effects of estradiol and progesterone on pulsatile luteinizing hormone (LH) secretion in the rat. In the first experiment, regularly cycling rats were ovariectomized on metestrus and a Silastic implant containing estradiol in oil (7.5, 15 or 30 micrograms/ml) or crystalline progesterone (0.7 or 3 cm long) was placed s.c. immediately after surgery. Rats were cannulated 3 days later and frequent blood samples collected (every 10 min for 4 h) the next day. Estradiol treatment alone produced a dose-dependent suppression in mean LH by decreasing LH pulse amplitude without altering interpulse interval. Progesterone treatment alone had no effect, but when the low progesterone dose was combined with a subthreshold estradiol treatment, the combination decreased LH pulse amplitude, but had no effect on the interval between pulses. The combination of high progesterone and low estradiol completely suppressed LH secretion. In the second experiment, rats were bled 7 days postovariectomy to increase the postcastration LH rise and examine higher steroid treatments. Three progesterone treatments (0.7, 1.5 and 3 cm long implants) were combined with the low estradiol treatment; the high estradiol dose (30 micrograms/ml) was also tested. All treatments decreased LH pulse amplitude without altering interpulse interval, although the highest progesterone treatment again completely suppressed LH in most rats so that no statistical analysis could be performed. No firm conclusions can be drawn about the effects of the high steroid treatments that completely suppressed LH; such an effect could reflect either inhibition of pulse frequency or amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)