Ovulations in rat ovaries perfused in vitro with follicle-stimulating hormone

Using the model of the isolated perfused rat ovary, we have found that highly purified ovine follicle-stimulating hormone (FSH) preparations cause ovulation and that this effect is not due to luteinizing hormone (LH) contamination. Ovine FSH-13 at a concentration of 1.5 mU/ml induced ovulations in all perfused ovaries (8.8 +/- 2.3 ovulations/ovary), as did a more purified preparation, ovine FSH-211B, at concentrations of 0.5 mU/ml (15.0 +/- 6.4 ovulations/ovary) and 5 mU/ml (11.3 +/- 2.6 ovulations/ovary). This ovulation-inducing effect of FSH is accompanied by a marked stimulation of estradiol levels in the perfusion medium without stimulation of progesterone levels. Furthermore, a purified rat FSH preparation (15 mU/ml) also induced ovulation in all ovaries (13.8 +/- 2.2 ovulations/ovary) as well as a stimulation of both estradiol and progesterone in the medium. These data clearly confirm the direct ovulatory effect of FSH on the ovary.     

Estradiol induces and progesterone inhibits the preovulatory surges of luteinizing hormone and follicle-stimulating hormone in heifers

Objectives were to determine: 1) whether estradiol, given via implants in amounts to stimulate a proestrus increase, induces preovulatory-like luteinizing hormone (LH) and follicle-stimulating hormone (FSH) surges; and 2) whether progesterone, given via infusion in amounts to simulate concentrations found in blood during the luteal phase of the estrous cycle, inhibits gonadotropin surges. All heifers were in the luteal phase of an estrous cycle when ovariectomized. Replacement therapy with estradiol and progesterone was started immediately after ovariectomy to mimic luteal phase concentrations of these steroids. Average estradiol (pg/ml) and progesterone (ng/ml) resulting from this replacement were 2.5 and 6.2 respectively; these values were similar (P greater than 0.05) to those on the day before ovariectomy (2.3 and 7.2, respectively). Nevertheless, basal concentrations of LH and FSH increased from 0.7 and 43 ng/ml before ovariectomy to 2.6 and 96 ng/ml, respectively, 24 h after ovariectomy. This may indicate that other ovarian factors are required to maintain low baselines of LH and FSH. Beginning 24 h after ovariectomy, replacement of steroids were adjusted as follows: 1) progesterone infusion was terminated and 2 additional estradiol implants were given every 12 h for 36 h (n = 5); 2) progesterone infusion was maintained and 2 additional estradiol implants were given every 12 h for 36 h (n = 3); or 3) progesterone infusion was terminated and 2 additional empty implants were given every 12 h for 36 h (n = 6). When estradiol implants were given every 12 h for 36 h, estradiol levels increased in plasma to 5 to 7 pg/ml, which resembles the increase in estradiol that occurs at proestrus. After ending progesterone infusion, levels of progesterone in plasma decreased to less than 1 ng/ml by 8 h. Preovulatory-like LH and FSH surges were induced only when progesterone infusion was stopped and additional estradiol implants were given. These surges were synchronous, occurring 61.8 +/- 0.4 h (mean +/- SE) after ending infusion of progesterone. We conclude that estradiol, at concentrations which simulate those found during proestrus, induces preovulatory-like LH and FSH surges in heifers and that progesterone, at concentrations found during the luteal phase of the estrous cycle, inhibits estradiol-induced gonadotropin surges. Furthermore, ovarian factors other than estradiol and progesterone may be required to maintain basal concentrations of LH and FSH in heifers.     

Differential effects of follicle-stimulating hormone and luteinizing hormone on Leydig cell function and restoration of spermatogenesis in hypophysectomized and photoinhibited Djungarian hamsters (Phodopus sungorus)

Effects of pure human follicle-stimulating hormone (hFSH) and ovine luteinizing hormone (oLH) on testicular function were investigated in long-term hypophysectomized or photoinhibited Djungarian hamsters. hFSH (5 IU) or oLH (5 micrograms) or a combination of FSH and LH (5 IU and 5 micrograms, respectively) were injected s.c. twice daily for 7 days to hypophysectomized and photoinhibited hamsters. Other photoinhibited hamsters were treated for 14 and 21 days with FSH and LH (3 IU and 3 micrograms, respectively) in a similar way. LH alone had little, if any, effect on testicular weights; FSH, when injected alone or in combination with LH (FSH/LH), caused a significant increase in testes weights at each time point. On the other hand, LH or FSH/LH, but not FSH alone, caused a significant increase in the accessory organ weights. FSH had no effect on intratesticular testosterone (T) or on 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity but enhanced the in vitro response of interstitial cells to hCG. LH and FSH/LH had pronounced effects on intratesticular T, 3 beta-HSD activity, and in vitro response of interstitial cells to human chorionic gonadotropin. Treatment with FSH or FSH/LH caused regrowth of the testis and restoration of tubular lumen and tubular diameter and restored complete spermatogenesis. However, LH had little effect on spermatogenesis in spite of increased intratesticular and peripheral T levels. These results indicate that although LH can cause a full redifferentiation of Leydig cells in photoinhibited hamsters, it has only minor effects on tubular function. On the other hand, FSH alone induces full restoration of tubular function in these animals and has no direct effect on Leydig cell steroidogenesis, but may enhance the Leydig cell responsiveness to LH.     

Estrogen production by fetal rat gonads

Aromatase activity in fetal rat testes and ovaries was demonstrated by the conversion of tritiated testosterone or 19-hydroxyandrostenedione into estrone and estradiol, which were identified and quantified by double isotopic dilution and recrystallization to constant specific activity. Testes formed mostly estradiol, ovaries mostly estrone. Aromatase activity was stimulated by cAMP in both the testes and ovaries as early as 17 days of fetal life. Stimulation by FSH was noted at this same stage in the testis, but not before 3–4 days after birth in the ovary. LH was without effect on aromatase activity in both kinds of gonads. Basal estrogen secretion was non-existent or undetectable in both the testes and ovaries in fetal stages. In the presence of cAMP and as early as 17 days of fetal life, the testes released estradiol, as early as 14 days the ovaries released estrone. Estrogen secretion was stimulated by LH and FSH at fetal stages in the testis and at infantile stages in the ovary. Responsiveness to gonadotrophins closely followed the appearance of the receptors.     

Effect of vitamin A deficiency upon gonadotropin response to gonadotropin-releasing hormone

There is a monotypic change in basal serum gonadotropin levels following retinol treatment of chronically vitamin A-deficient (VAD) male rats. The present study was undertaken to investigate the hypothesis that the specific increase in serum follicle-stimulating hormone (FSH) represents a change in gonadotrope responsiveness to gonadotropin-releasing hormone (GnRH). To this end, a test dose of GnRH was given to VAD rats pre-, 5 days post-, and 10 days postreplacement of vitamin A (PVA). In VAD rats, basal serum FSH and luteinizing hormone (LH) levels were higher than those of controls. Increased LH/testosterone ratios, both in basal levels and in the secretory response to GnRH, suggested Leydig cell hyporesponsiveness in VAD animals. Both the FSH and LH responses to GnRH were maximal at 1 h, declining thereafter. Although the absolute increments in FSH and LH 1 h after GnRH in VAD rats were greater than in controls, the percent increase in FSH tended to be lower in VAD rats and to increase after vitamin A replacement. The specific enhancement of FSH release PVA became evident only when assessing total secretion of FSH and LH after GnRH. Luteinizing hormone response to GnRH increased PVA, but not significantly, while FSH secretion after GnRH increased both 5 and 10 days PVA, times during which basal FSH levels were also increasing. These changes in FSH secretion could not be attributed either to increases in endogenous GnRH or to changes in testosterone or estradiol levels. Basal serum androgen binding protein levels, elevated in VAD animals, did not respond to the acute increases in FSH after GnRH and remained high PVA, suggesting no acute change in Sertoli cell function. Thus, the PVA increase in FSH secretion unmasks a partial inhibition of the gonadotrope present in the retinol-deficient, retinoic acid-fed male rat.     

Testicular development, histology, and hormone profiles in three yearling angus bulls with spermatogenic arrest

This article discusses the interactions between testis criteria and hormone profiles in Angus bulls with spermatogenic arrest. From 2 to 12 months (mo), testis diameter and hormone concentrations (basal and GnRH-stimulated) were evaluated in 27 bulls. At 12 mo, testes were excised. The z statistical test was used to determine whether parameters in three infertile bulls were different (P < 0.05) from those in 24 bulls with normal spermatouenesis. Bull 1 had Sertoli cell-only syndrome and Bull 2 had 90% of the tubules without germ cells and only A1 spermatogonia in the remaining. In Bull 3, germ cells did not advance beyond the primary spermatocyte stage. At 12 mo, testes of Bull 1 (99 g), Bull 2 (105 g) and Bull 3 (32 g) weighed less than those of normal bulls (251.5 +/- 56 g). Sertoli cell numbers/testis in Bull 1 (3.8 x 10(9)) and Bull 2 (4.3 x 10(9)) were not different from those in normal bulls (4.9 +/- 0.3 x 10(9)), but were reduced in Bull 3 (1.6 x 10(9)). The number of Leydig cells per gram of testis parenchyma was higher in Bull 1 (5.4 x 10(7)), Bull 2 (7.3 x 10(7)) and Bull 3 (19 x 10(7)) than in normal bulls (3.6 +/- 0.2 x 10(7)). In Bulls 1 and 2, basal and GnRH-stimulated LH, FSH, testosterone (T), androstenedione (delta4A) and estradiol 17-beta (E2) were within normal ranges at most ages. However, basal FSH and LH were greater in Bull 3 than in normal bulls, probably the causes for higher Leydig cell density. Also in the same animal, GnRH induced lower responses in LH and FSH, consequence of low basal T and E2 at some ages. Basal and GnRH-stimulated delta4A in Bull 3 were greater than in normal bulls after 6 mo, indicating impairment of Leydig cell differentiation. Deficiency in hormone secretion did not appear to be the cause of infertility, which points toward impaired gonadal responses or secretion of intratesticular factors, or genetic defects. Moreover, infertile animals may not always show pronounced changes in hormone secretion, but evaluation of testis growth around puberty can help identify those animals that do not have proper gonadal development.     

Mechanisms involved in the ability of human chorionic gonadotropin to increase the responsiveness of the infant rat's testis to follicle-stimulating hormone

Pretreatment of 9-day-old rats for 3 days with human chorionic gonadotropin (hCG) increases the amount of estradiol secreted by the testis in response to in vivo or in vitro stimulation with follicle-stimulating hormone (FSH). Potential mechanisms for this sensitizing effect were studied by treating infant rats with a variety of agents and then using radioimmunoassay to determine testicular estradiol secretion. Substitution of 3 days priming with estradiol for hCG did not enhance subsequent in vitro responsiveness to FSH. Subcutaneous capsules of 1,4,6-androstatriene-3,17-dione (ATD) blocked stimulation of testicular aromatization in vivo by hCG or FSH. ATD capsules alone, or when combined with the antiestrogen tamoxifen, were not able to alter the ability of hCG pretreatment to increase responsiveness to in vitro FSH. It was concluded that estradiol was not involved in the sensitization caused by hCG in this model system. When gonadal tissue from 12-day-old rats was incubated in the presence or absence of 0.6 microM testosterone and various concentrations of FSH, more estradiol was secreted by testes in the containing testosterone. The amount secreted was not different from that noted after hCG priming. Priming of 9-day-old rats for 3 days with the nonaromatizable androgen 5 alpha-dihydrotestosterone did not influence the amount of estradiol secreted in response to FSH. It is further concluded that hCG augments the testicular aromatization response of infant rats to FSH by providing additional substrate for these reactions.     

Possible involvement of inhibin in altered follicle-stimulating hormone (FSH) secretion during dissociated luteinizing hormone (LH) and FSH release: unilateral castration and experimental cryptorchidism

Male rats were either unilaterally or bilaterally castrated, or were rendered cryptorchid when they were either 15 or 45 days old. Subsequently, blood was sampled over the next several weeks and plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), and immunoreactive inhibin-alpha (irI alpha) levels were measured by specific radioimmunoassays (RIAs). At the end of the experiment, gonadal expression of inhibin-alpha, inhibin-beta A, and inhibin-beta B subunits was measured by S1 nuclease analysis and in situ hybridization. In both age groups, bilateral castration (BC) produced the expected marked (p less than or equal to 0.01) increases in plasma LH and FSH levels, and concomitant decreases in T and irI alpha secretion within 1 - 2 days after surgery. In 15-day-old animals, unilateral castration (UC) significantly increased FSH and decreased circulating levels of irI alpha, but did not measurably alter LH or androgen production. At 7 days after surgery, the level of inhibin mRNA in the remaining testis was unchanged. In 45-day-old animals, UC caused a measurable increase in FSH, with little or no changes in the circulating levels of irI alpha. Plasma T levels were lowered (p less than or equal to 0.05) by UC; however, there were no statistical changes in LH levels in these UC rats. Finally, T administration markedly reversed UC-induced increase in FSH secretion in both age groups. Androgen therapy also interfered with inhibin release in 45-day-old, but not in 15-day-old rats. In rats 15 days old at the time of surgery, cryptorchidism produced a small but measurable increase (p less than or equal to 0.05) in LH release at Week 6 only, which was accompanied by a significant (p less than or equal to 0.01) decline in T secretion. Plasma FSH levels were elevated at all times in cryptorchid rats, and at 2, 4, and 6 wk, these levels were not statistically distinguishable (p greater than 0.05) from those of castrated animals. In this group of rats, cryptorchidism caused a transient increase (p less than or equal to 0.05) in irI alpha values 1 wk after surgery, but no changes at later times. Finally, measurement of testicular inhibin-alpha subunit messenger RNA (mRNA) levels showed an approximately 2-fold increase compared to total RNA levels in the testis. However, because of the significant decrease in total RNA levels per testis caused by cryptorchidism, the absolute change in inhibin-alpha subunit mRNA levels per testis corresponded to an approximately 3-fold decrease.(ABSTRACT TRUNCATED AT 400 WORDS)     

Seasonal changes in the endocrine responsiveness of the pituitary and tests of male sheep in relation to their patterns of gonadotropic hormone and testosterone secretion

Pituitary and testicular endocrine responses to exogenous gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH), respectively, were assessed for adult rams in an investigation of the regulation of seasonal changes in the patterns of episodic LH and testosterone secretion. Concurrent variations in testis size and in circulating levels of follicle stimulating hormone (FSH) and prolactin (PRL) were also examined. On 10 occasions throughout the year, serum hormone levels were assessed over 6- to 8-h periods during which time rams were left untreated (day 1) or were injected (iv) with single doses of either 10 micrograms synthetic GnRH (day 2) or 30 micrograms NIH-LH-S18 (day 3); blood samples were collected from the jugular vein at 10- to 20-min intervals. Testicular redevelopment during the summer, as indicated by increasing testis diameter measurements, was associated with increases in mean FSH level and was preceded by a springtime rise in mean PRL level; "spontaneously" occurring LH pulses and those produced in response to GnRH treatment were relatively large during this period. Increases in the magnitude of testosterone elevations in response to both endogenously and exogenously produced LH pulses occurred in August. Mean testosterone levels were elevated fourfold in the fall as a consequence of relatively frequent and small LH pulses stimulating a more responsive testis to produce more frequent and larger testosterone elevations; endogenous LH pulses, however, did not appear to stimulate the testes maximally at this time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Organ culture of mammalian testis. III. Inhibin secretion.

Mouse testes were cultured for 19--20 days at either 31 or 37 degrees C with a change of medium every 4 days. After treatment with charcoal and dextran T, the recovered testis media were incubated with rat anterior pituitary cells, and secretions of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were estimated by radioimmunoassay 3 days later. FSH release was significantly lowered when pituitary cells were grown with media of testes cultured 31 degrees C compared to cultures grown with fresh medium or with media of testes cultured at 37 degrees C for more than 4 days. LH secretion was normal in one experiment and reduced in the other with the media of testes cultured at 31 degrees C. Treatment of testicular media by heat or trypsin reduced the inhibiting activity. After 8 days at 37 degrees C, both germinal and Sertoli cells were damaged in the testis cultures, while at 31 degrees germinal cells alone were destroyed, Sertoli cells remained normal. These studies suggest that (1) a substance which responds to the definition of inhibition (protein--preferentially acting on FSH) is secreted in the medium of testis culture; (2) inhibin is produced by Sertoli cells; (3) inhibin is secreted only if the temperature is inferior to 37 degrees C.     

Effect of cyanoketone on follicle-stimulating hormone (FSH) induction of receptors for FSH in granulosa cells of the rat

Follicle-stimulating hormone (FSH) enhances the conversion of testosterone or androstenedione into estradiol by stimulating the aromatase enzyme system. Estradiol also enhances FSH action. Thus, a synergistic action of FSH and estradiol may be required for maturation of ovarian follicles. We hypothesized that estradiol may be required for FSH action. Thus, blocking estrogen synthesis should prevent FSH-induced increases in FSH receptors. Hypophysectomized rats were divided into five groups and injected subcutaneously with: 1) saline, 2) cyanoketone (0.05 mg, blocks the conversion of pregnenolone to progesterone), 3) ovine FSH (oFSH, 200 micrograms), 4) cyanoketone then oFSH 24 h later, or 5) cyanoketone plus estradiol [or progesterone, testosterone, promegestrone (R5020), dihydrotestosterone (DHT), 2 mg], then FSH 24 h later. Animals were decapitated at 0, 12 or 24 h after an injection of oFSH, and membrane receptors for FSH and luteinizing hormone (LH), plus nuclear receptors for estradiol from granulosa cells, were measured. LH receptor levels were increased only after administration of FSH and estradiol. At 0 and 24 h, numbers of FSH or estradiol receptors were similar in saline- and cyanoketone-treated animals. FSH alone increased (P less than 0.01) FSH and estradiol receptors 3-fold and 4-fold, respectively, over controls by 12 and 24 h. Cyanoketone prevented these increases in FSH and estradiol receptors. Estradiol replacement fully reversed the effects of cyanoketone on FSH action. Replacement with progesterone and testosterone was able to only partially restore levels of FSH receptors; however, estradiol receptor numbers were also increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Interaction of season and estradiol in the regulation of gonadotropin secretion in the adult ram

The effects of season and estradiol on the secretion of gonadotropic hormones in adult Dorset X Leicester X Suffolk rams were studied. Control groups of intact and castrate rams, and castrate rams given estradiol replacement (approximately 11.5 pg/mL) via polydimethylsiloxane capsules (sc) were assessed for 1 year, beginning in August. Mean concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL) were determined every 2 weeks for all three groups of rams and measurements of testosterone concentration and scrotal circumference were taken on the intact rams. Pulsatile LH release and the LH response to a 2-micrograms dose (iv) of gonadotropin-releasing hormone (GnRH) were assessed for all rams when the testes of intact rams were redeveloped (late October), regressed (early February, late April), and redeveloping (early August). Season directly affected LH-pulse amplitude, which increased only in the control castrate rams between February and April. In October, LH-pulse frequency was the same in both groups of castrate rams, while in April, frequency in the estradiol-treated castrate rams was suppressed to intact ram values. Pituitary responsiveness to exogenous GnRH did not change throughout the year in either of the castrate groups, but along with LH-pulse amplitude, it was increased in August in the intact rams. Although FSH secretion was 14-fold higher in the control castrate rams than in the intact rams, seasonal-directional changes in mean concentration were similar. FSH concentration in the estradiol-treated castrate rams was stable throughout the year. PRL secretion never differed between the control castrate and intact rams but was enhanced in the estradiol-treated castrate rams, particularly during long days.     

Selective release of follicle-stimulating hormone by 5 alpha-dihydroprogesterone in immature ovariectomized estrogen-primed rats

The effect of 5 alpha-dihydroprogesterone (5 alpha-DHP) on gonadotropin release was examined in the immature acutely ovariectomized (OVX) rat primed with a low dose of estradiol (E2). Treatment with various doses of 5 alpha-DHP given in combination with E2 increased levels of follicle-stimulating hormone (FSH) but had no effect on serum luteinizing hormone (LH). A single injection of a maximally stimulating dose of 5 alpha-DHP (0.4 mg/kg) stimulated increases in serum FSH at 1200 h and, 6 h later, at 1800 h. Pituitary LH and FSH content was dramatically enhanced by 1600 h and levels remained elevated at 1800 h. The administration of pentobarbital at 1200 h, versus 1400 h or 1600 h, prevented the increase in basal serum FSH levels at 1800 h, implying that the release of hypothalamic LH releasing hormone (LHRH) is modulated by 5 alpha-DHP. In addition, changes in pituitary sensitivity to LHRH as a result of 5 alpha-DHP were measured and a significant increase in the magnitude of FSH release was observed at 1200 h and 1800 h. Although the LH response to LHRH in 5 alpha-DHP-treated rats was not different from controls, the duration of LH release was lengthened. These results suggest that 5 alpha-DHP may stimulate FSH release by a direct action at the pituitary level. Together, these observations support the theory that 5 alpha-DHP mediates the facilitative effect of progesterone on FSH secretion and further suggests an action of 5 alpha-DHP in this phenomenon at both pituitary and hypothalamic sites.     

Transitory increases of luteinizing hormone and follicle-stimulating hormone following luteectomy in hemiovariectomized primates significantly increase progesterone secretion in vitro by the subsequent corpus luteum

Ten chronically hemiovariectomized cynomolgus and rhesus monkeys were luteectomized 5.5 +/- 0.3 days after the midcycle luteinizing hormone (LH) and follicle-stimulating hormone (FSH) surge in two consecutive cycles. The corpus luteum (CL) was removed, weighed, dispersed with collagenase and the luteal cells counted. Luteal cells (50,000/ml) were incubated in Ham's F10 medium for 3 h at 37 degrees C either in the presence or absence of 100 ng/ml human chorionic gonadotropin (hCG). Daily blood samples were taken from the monkeys throughout the study for determination of LH, FSH, estradiol (E2) and progesterone levels. Within 5 days following each luteectomy (LX), all monkeys responded with a significant increase in FSH and LH (P less than 0.05). Ovulatory LH/FSH surges occurred 14.4 +/- 0.5 days after the first LX. Hormonal profiles of serum progesterone prior to the first and second LX, CL weight and number of luteal cells/CL were similar (P greater than 0.05). However, luteal cells obtained at the second LX produced more progesterone (P less than 0.05) in vitro under basal and hCG-stimulated conditions than cells from the first LX. The areas under the LH and FSH curves following the first LX were highly correlated (P less than 0.05) with the in vitro progesterone production following the second LX. Thus, the monkeys with the largest areas under the LH and FSH curves subsequently had the highest in vitro progesterone production.     

Effect of castration on plasma concentrations of luteinizing hormone and follicle-stimulating hormone in adult Merino rams which were homozygous carriers or non-carriers of the Booroola fecundity gene

Before castration, the mean plasma concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) did not differ between FF and ++ Booroola rams. After castration, mean LH and FSH concentrations increased after 8 h, and for the next 14 days the rate of increase in FSH, but not LH, secretion was significantly faster in FF than in ++ rams (P less than 0.05). Mean FSH concentrations over this period were significantly higher in FF than in ++ rams (P less than 0.05). In both genotypes, the ranked FSH values did not significantly change their order over time, i.e. a significant within-ram effect was noted (P less than 0.05). Repeated-measures analysis of variance indicated a significant effect of genotype on mean FSH secretion (P less than 0.05) and a significant effect of sire in the FF (P less than 0.05), but not the ++ (P = 0.76), genotype. From Day 28 to Day 58 after castration, FSH and LH concentrations were variable and no overall increases in concentrations were observed. The mean concentrations of both hormones over this period were not related to genotype. There were no gene-specific differences in pulsatile LH secretion 14 weeks after castration. However, the mean LH, but not FSH, response to a bolus injection of 25 micrograms of gonadotrophin-releasing hormone (GnRH) was significantly higher in FF than in ++ rams (P less than 0.05) and this was not significantly affected by sire. These studies support the hypothesis that the F gene is expressed in adult rams, in terms of pituitary responsiveness to an injection of GnRH and to the removal of the testes, but it is not clear from this study whether the influence of sire is related to or independent of the apparent gene-specific differences.     

The inhibitory action of corticotropin-releasing hormone on gonadotropin secretion in the ovariectomized rhesus monkey is not mediated by adrenocorticotropic hormone

Earlier observations in our laboratory indicated that i.v. infusion of human/rat corticotropin-releasing hormone (hCRH) suppresses pulsatile luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release in ovariectomized rhesus monkeys. Since cortisol secretion increased significantly as well, it was not possible to exclude the possibility that this inhibitory effect of hCRH on gonadotropins was related to the activation of the pituitary/adrenal axis. The purpose of the present study was to determine the role of pituitary/adrenal activation in the effect of hCRH on LH and FSH secretion. We compared the effects of 5-h i.v. infusions of hCRH (100 micrograms/h, n = 7) and of human adrenocorticotropic hormone (ACTH) (1-24) (5 micrograms/h, n = 3; 10 micrograms/h, n = 3, 20 micrograms/h, n = 3) to ovariectomized monkeys on LH, FSH, and cortisol secretion. As expected, during the 5-h ACTH infusions, cortisol levels increased by 176-215% of baseline control, an increase similar to that observed after CRH infusion (184%). However, in contrast to the inhibitory effect observed during the CRH infusion, LH and FSH continued to be released in a pulsatile fashion during the ACTH infusions, and no decreases in gonadotropin secretion were observed. The results indicated that increases in ACTH and cortisol did not affect LH and FSH secretion and allowed us to conclude that the rapid inhibitory effect of CRH on LH and FSH pulsatile release was not mediated by activation of the pituitary/adrenal axis.     

Effects of steroid administration on pituitary luteinizing hormone and follicle-stimulating hormone in ovariectomized pony mares in the early spring: pituitary responsiveness to gonadotropin-releasing hormone and pituitary gonadotropin content

These experiments tested the hypothesis that administration of steroid hormones to ovariectomized (OVX) mares during the vernal transition to the breeding season would influence LH and FSH secretion. Circulating gonadotropin concentrations, response to exogenous GnRH, and pituitary gonadotropin content were monitored. Experiments 1 and 2 were conducted, beginning 10 March, and 3 February, respectively, utilizing a total of 30 long-term OVX pony mares. In experiment 1, mares were administered vehicle (n = 5) or estradiol-17 beta (E2, n = 5, 5 mg/3 ml sesame oil), twice daily for 16 days. Blood samples were collected daily for assessment of circulating LH and FSH concentrations. On Day 10 of treatment, 400 micrograms GnRH were administered to all mares. LH increased significantly over days of treatment in the estradiol-treated group, but pituitary response to GnRH tended to be less than in control mares. Circulating FSH tended to decline over days of treatment in estradiol-treated mares, and the pituitary response to GnRH was significantly reduced. Pituitary LH, but not FSH, was increased on Day 16 of treatment with estradiol. In experiment 2, 20 OVX mares received, twice daily, vehicle (n = 5), E2, n = 5; 5 mg), progesterone (P4, n = 5; 100 mg), or progesterone plus estradiol (P4/E2, n = 5; 100 + 5 mg). Treatment continued for 14 days. GnRH (100 micrograms) challenges were administered on Days 6 and 13 of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Stimulatory effect of follicle-stimulating hormone on rat Leydig cells

Summary The effects of FSH on the testicular interstitial tissue of immature hypophysectomized rats were studied by comparing morphological changes in Leydig cells with quantitative changes in interstitial tissue histology using morphometric analysis. Three groups of rats received subcutaneous injections of 0.5 ml saline vehicle or 10 g rFSH or 20 ng oLH (equivalent to the amount of LH known to contaminate the FSH), twice daily for 7 days. Administration of FSH significantly increased testis weight and stimulated more advanced spermatogenesis compared to saline or LH. Morphometric analysis of testes of LH-treated rats showed a small but significant increase in total interstitial cell volume compared to saline treatment. FSH caused much greater increases in the total volume of interstitial tissue and interstitial cells than either saline or LH and significantly increased the total volume of interstitial fluid by comparison with the other groups. FSH but not saline or LH treatment resulted in a striking hypertrophy of Leydig cells, to produce cells ultrastructurally identical to Leydig cells from adults. Since the target tissue of FSH is the seminiferous epithelium, the observed effects on Leydig cells by FSH treatment suggest that the secretion of factors by the seminiferous tubules may mediate the maturation of Leydig cells.     

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.