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PubMed1998

The in vitro effect of leptin on basal and growth hormone-releasing hormone-stimulated growth hormone secretion from the ovine pituitary gland.

We have studied the direct effect of leptin on the secretion of GH from the anterior pituitary gland of the sheep. Using primary cultures of ovine pituitary cells, leptin (10(-9)-10(-7) M) treatment for 30 min did not affect basal or GHRH (10(-7) M)-stimulated GH secretion. Following treatment for 24 h, a dose of 10(-7) M leptin stimulated basal GH secretion. In contrast, doses of 10(-7) and 10(-8) M leptin inhibited GHRH-stimulated GH secretion after 24 h of treatment. These results suggest that leptin can have long-term effects on the somatotropes, but no acute effect. Furthermore, leptin appears to have opposite effects on basal and GHRH-stimulated GH secretion.

Animals↗
PubMedDate not supplied

Growth hormone secretion in Alzheimer's disease: studies with growth hormone-releasing hormone alone and combined with pyridostigmine or arginine.

There is evidence that GH secretion is reduced in normal elderly subjects as well as in patients with Alzheimer's disease (AD). To clarify the mechanisms underlying this GH hyposecretory state in 14 elderly subjects (age 65-75 years) and 15 AD patients (age 61-78 years), we studied the effects of both pyridostigmine (PD, 120 mg orally), a cholinesterase inhibitor, and arginine (ARG, 0.5 g/kg i.v.), two substances likely acting via inhibition of hypothalamic somatostatin, on GH response to GHRH (1 microgram/kg i.v.). The GH response to PD alone was also studied. Twenty-two young healthy volunteers were studied as control group. Basal GH levels were similar in young, elderly and AD subjects (0.7 +/- 0.2, 0.8 +/- 0.2 and 0.9 +/- 0.2 microgram/l). IGF-I levels were lower (p < 0.005) in elderly (73.9 +/- 8.2 microgram/l) and in AD subjects (108.0 +/- 5.9 micrograms/l) than in young subjects (288.7 +/- 22.1 micrograms/l); however, they were higher (p < 0.01) in AD patients than in the elderly subjects. The PD-induced GH release did not significantly differ in young, elderly and AD subjects while the GH responses to GHRH in the elderly (AUC: 297.9 +/- 49.2 micrograms/l) and in AD subjects (437.6 +/- 93.5 micrograms/l/h) were lower (p < 0.01) than in young subjects (658.6 +/- 100.1 micrograms/l/h). PD potentiated the GH response to GHRH both in elderly and in AD subjects (901.7 +/- 222.4 and 1,070.3 +/- 207.2 micrograms/l/h, p < 0.005) but these responses were lower (p < 0.0001) than those recorded in young subjects (2,041.1 +/- 245.6 micrograms/l/h).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Growth hormone-releasing hormone-induced growth hormone secretion in adult rats orchidectomized or injected with ethylene dimethane sulphonate.

It is well known that GHRH-induced GH secretion decreases after orchidectomy. To verify if testicular factors other than testosterone are involved in this effect, the GHRH-induced GH secretion and testosterone plasma levels were compared in adult male rats that were either intact, treated with ethylene dimethane sulphonate (EDS) (a specific toxin for Leydig cells), orchidectomized or testosterone-treated orchidectomized. We found that testosterone plasma levels and ventral prostate weight decreased to a similar extent in orchidectomized and EDS-treated males. GHRH-induced GH secretion only decreased in orchidectomized males. We conclude that testicular factors, other than androgens, increase GHRH-induced GH secretion.

Animals↗
PubMed1991

Growth hormone regulation by growth hormone-releasing hormone in infant rhesus monkeys.

To study the relationship of endogenous GHRH to the changes seen in serum GH concentration in neonatal primates, we administered antiserum to GHRH (GHRH-Ab) or GHRH antagonist, (N-Acetyl-Tyr1,D-Arg2)GHRH-(1-29)-NH2, to unanesthetized, fasted rhesus monkeys, 1-31 days of age, via an acutely placed venous catheter. The administration of GHRH-Ab resulted in a significant decrease in serum GH concentration at 1-2 and 7-9 days, but not at 28-31 days of age. The administration of GHRH antagonist resulted in a significant decrease in serum GH concentrations at 1-2 days, but not at 7 or 14 days of age. These results imply that basal serum GH is more dependent on endogenous GHRH at 1-2 days than after 7-28 days of age. This suggests developmental changes in the hypothalamic regulation of GH secretion with advancing age in the neonatal period.

Animals↗
PubMed1981

Regulation of the second surge of follicle-stimulating hormone; effects of antiluteinizing hormone-releasing hormone serum and pentobarbital.

The blockade in the rat of the estrous FSH surge was investigated by the injection of anti-LHRH serum in order to clarify whether LHRH controls this postovulatory surge as well as the preovulatory LH-FSH surge. A single iv injection of anti-LHRH serum at 1300 h on proestrus not only inhibited ovulation but also eliminated both the preovulatory LH-FSH surge and the second FSH surge in estrus. A single iv injection of anti-LHRH serum at 2200 h on proestrus after the LH-FSH surge did not inhibit either the estrous FSH surge or ovulation, although plasma LH was lowered, and the number of ova ovulated was reduced. Depression of plasma FSH and LH levels was also observed after a single iv injection of pentobarbital sodium (Nembutal; 35 mg/kg BW) at 1300 h on proestrus, but no such effect was observed when pentobarbital was injected at 2200 h on proestrus. A single injection of 10 IU hCG at 1800 h on diestrous II induced precocious ovulation and a concomitant increase in FSH secretion. It was not possible to inhibit the induced secretion of FSH and ovulation by a simultaneous injection of anti-LHRH serum, but plasma LH was completely suppressed. These results demonstrate that the second FSH surge is not controlled by LHRH.

Animals↗
PubMed1983

Involvement of hypothalamic luteinizing hormone-releasing hormone in the regulation of the estrous follicle-stimulating hormone surge in the female golden hamster.

Hypothalami collected from female hamsters during proestrus and estrus were assessed for LHRH content by bioassay and RIA. During estrus, as serum FSH levels rose, a depletion of hypothalamic LHRH was observed. The pattern of hypothalamic LHRH accumulation and depletion during proestrus and estrus as well as changes in serum and pituitary FSH concentrations were altered as a result of phenobarbital administration at 1200 h on proestrus. The effects of phenobarbital upon hypothalamic LHRH content as well as serum and pituitary FSH concentrations were overridden by the injection of purified FSH into the third ventricle of the hypothalamus at 1500 h during proestrus. The results of the present study suggest that the estrous FSH surge in hamsters is mediated, at least in part, by a concurrent discharge of hypothalamic LHRH. Further, intraventricular injection of FSH elicits a selective increase in serum FSH during estrus by influencing this LHRH-dependent system.

Animals↗
PubMed1985

Effects of glucocorticoids on responsiveness of luteinizing hormone and follicle-stimulating hormone to gonadotropin-releasing hormone by male rat pituitary cells in vitro.

To determine if the inhibitory effects of glucocorticoids on GnRH-stimulated secretion of LH observed in male rats in vivo are exerted directly on the pituitary, dispersed pituitary cells from adult male rats were treated with 60 or 600 ng/ml cortisol (F) or corticosterone (B) during one or two 48-h incubations. Control cells received no glucocorticoids. During the second 48 h, some cells from each group were treated with GnRH (2.4 X 10(-11)-6.2 X 10(-8) M). Concentrations of LH and FSH in media and cells were measured by RIA. Treatment with steroids had no effect on basal secretion or maximal GnRH-stimulated secretion of LH, or on maximal secretion of FSH. Treatment with 600 ng/ml B for 96 h increased basal secretion of FSH relative to controls. All treatments with glucocorticoids increased the slopes of the GnRH dose-response curves for both LH and FSH, cell content of LH, total (cells + medium) LH, and total FSH. Incubation with 6 micrograms/ml F or B or 60 ng/ml dexamethasone gave similar results. Decreasing the time period of the second incubation to 6 h results in no significant differences between control cells and cells treated with B or F. These results show that glucocorticoids have different effects in vivo and in vitro, suggesting that inhibitory effects of glucocorticoids on secretion of LH in vivo may not be exerted directly on the pituitary but are exerted elsewhere, perhaps by altered hypothalamic secretion of GnRH. Also, these results show that male and female pituitaries in vitro respond differently to glucocorticoids.

Animals↗
PubMed1985

Differential regulation of pulsatile luteinizing hormone (LH) and follicle-stimulating hormone secretion in ovariectomized rats disclosed by treatment with a LH-releasing hormone antagonist and phenobarbital.

Although pulsatile LH release in ovariectomized (OVX) rats appears to be controlled by pulsatile discharges of LHRH, the neuroendocrine regulation of episodic FSH release remains to be explored. The main objective of the present study is to compare and contrast the effects of a potent LHRH antagonist (ALHRH) and a central nervous system depressant, phenobarbital (PhB), on pulsatile LH and FSH release in OVX rats. Three to 4 weeks after ovariectomy, blood samples were obtained at 10-min intervals for 3 h, after which LHRH was injected and sampling continued for an additional hour. In control OVX rats, periodic increases in plasma LH and FSH levels occurred approximately every 30 to 60 min, respectively. Treatment of OVX rats with PhB several hours earlier resulted in a suppression of mean plasma levels and pulse frequencies of both LH and FSH. Interestingly, PhB suppressed the pulse amplitude of LH, but not of FSH. Phenobarbital increased pituitary LH responses to LHRH, but did not alter the FSH responses. When ALHRH was given to OVX rats 24 h before blood sampling, mean plasma LH levels as well as LH pulse frequency and amplitude were severely diminished. In striking contrast, ALHRH did not affect the frequency or amplitude of FSH pulses. However, mean plasma FSH levels were suppressed to 31% of levels measured in control OVX rats. These results demonstrate that in contrast to LH secretion, FSH secretion in OVX rats appears to be regulated by two distinct neuroendocrine mechanisms: an LHRH-dependent mechanism controlling the nonepisodic component of FSH secretion (baseline secretion) and a LHRH-independent mechanism controlling pulsatile FSH release.

Animals↗
PubMed1986

Evidence that pulsatile follicle-stimulating hormone secretion is independent of endogenous luteinizing hormone-releasing hormone.

Although LHRH can stimulate the release of both LH and FSH from the pituitary, there are a number of instances in which the secretion of LH and FSH are divergent. Previous studies from our laboratory have indicated that pulsatile LH and FSH secretion are independently regulated by gonadal factors. We have, therefore, reexamined the role of LHRH in regulating pulsatile gonadotropin secretion by evaluating the effect of passive LHRH immunoneutralization on LH and FSH secretion in castrate adult male rats. Injection of 500 microliters ovine anti-LHRH serum no. 772 (LHRH-AS) into 2-week-castrate rats caused an 85% suppression of mean plasma LH levels by 2 h, which lasted through 48 h. Mean plasma FSH, however, was reduced by only 19% after 2 h and by only 59% after 48 h. When cannulated 2-week-castrate rats were bled every 10 min, both LH and FSH were secreted in a pulsatile manner. Injection of 500 microliters LHRH-AS caused an immediate abolishment of LH pulses and a rapid reduction in mean plasma LH through 24 h. Pulsatile FSH secretion, as characterized by the parameters of pulse frequency and amplitude, was unaffected by LHRH-AS, although mean plasma FSH levels were significantly reduced. Collectively, the results suggest that pulsatile FSH secretion is regulated by a separate factor(s) distinct from LHRH, but that LHRH is required for the maintenance of elevated FSH levels.

Animals↗
PubMed1987

Pulsatile follicle-stimulating hormone secretion is independent of luteinizing hormone-releasing hormone (LHRH): pulsatile replacement of LHRH bioactivity in LHRH-immunoneutralized rats.

We recently reported that passive immunoneutralization of endogenous LHRH in castrate male rats completely abolishes pulsatile LH secretion and, within 1 h, lowers mean plasma LH by 86%. While pulsatile FSH secretion, in terms of pulse amplitude and frequency, is not affected, mean plasma FSH is gradually lowered but only by 49% after 24 h. In the present study, we have examined the effect of replacing pulsatile LHRH biological activity on LH and FSH secretion in 4-week castrate male rats in which endogenous LHRH has been immunoneutralized by ovine anti-LHRH serum 772 (LHRH-AS) for 24 h. The LHRH-AS requires the 3-10 amino acid sequence of LHRH including the amidated C terminus for complete recognition. In order to circumvent the antiserum blockade, we utilized the LHRH agonist [Des Gly10]-LHRH ethyl amide (DG-LHRH) which is minimally recognized by the LHRH-AS but which possesses 2.6-fold the LH-releasing activity of LHRH. Twenty-four hours after injecting 500 microliter LHRH-AS into cannulated, castrate rats, sequential blood samples were taken every 10 min for 4 h. Bolus 3-ng injections of either DG-LHRH or saline were given iv either every 30 min during the 4-h collection period or every 30 or 60 min for 10 h before the initiation of and continuing through the 4-h collection period. Each DG-LHRH injection stimulated the release of a single pulse of LH, while pulsatile FSH secretion was unaffected. No synchrony was observed between the DG-LHRH pulses and the endogenous FSH pulses. Short term DG-LHRH treatment partially restored, and long term DG-LHRH treatment every 60 min completely restored, mean plasma FSH to the level observed in nonantiserum-treated castrate control rats. Long term DG-LHRH treatment every 30 min caused a rise in mean plasma FSH which exceeded the plasma FSH level of the nonantiserum-treated controls. The mean plasma level of LH was entirely dependent on the frequency of the DG-LHRH injection. The results of this study clearly demonstrate that pulsatile FSH secretion is independent of LHRH but that LHRH is required to elevate and/or maintain high mean plasma FSH levels. Trough levels of LH, however, are dependent on the frequency of LHRH-induced pulsatile LH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Simultaneous measurement of luteinizing hormone (LH)-releasing hormone, LH, and follicle-stimulating hormone release in intact and short-term castrate rats.

The temporal relationship between LHRH release and gonadotropin secretion as well as the effects of castration on LHRH release were investigated in conscious, freely moving male rats. LHRH release was measured in hypothalamic/median eminence perfusates, while levels of pituitary gonadotropins (LH, FSH) were determined in sequential blood samples obtained via atrial catheters. Twenty-four to 26 h before experiments, rats underwent sham surgery or castration. LHRH release in push-pull perfusates from both groups was pulsatile, and nearly all identified LH pulses (83.3%) were temporally associated with LHRH pulses. Of the fewer irregular FSH pulses that were observed, only 43.7% were temporally associated with LHRH pulses. Mean LHRH pulse amplitude and mean LHRH levels were not different in intact and castrate animals. The frequency of LHRH pulses was moderately increased in castrate rats (1.30 pulses/h) compared to that in intact animals (0.83 pulses/h), and this acceleration was accompanied by a significant increase in LH pulse frequency, pulse amplitude, and mean level. It was also noted that the number of silent LHRH pulses (those not associated with LH pulses) was dramatically reduced in castrate animals. Characteristics of gonadotropin release (pulse frequency, pulse amplitude, and mean level) were not significantly different in animals undergoing push-pull perfusion/bleeding procedures from those in rats not receiving push-pull cannula implants. We conclude from these studies that 1) LH pulses show a high concordance with LHRH pulses, providing evidence that the LHRH pulse generator operates as the neural determinant of LH pulses in male rats, 2) FSH secretion is not associated with LHRH release in an obvious and consistent manner, suggesting that LHRH/FSH relationships are not easily discerned in these animals or that a FSH-releasing factor distinct from the LHRH decapeptide may regulate FSH secretion, 3) a modest increase in LHRH pulse frequency occurs 24-30 h after castration, and 4) silent LHRH pulses occur with much greater regularity in intact than in castrate rats. The latter two observations suggest that both hypothalamic and intrapituitary sequelae of castration may be critically important in the development of postcastration increases in LH secretion and the negative feedback of gonadal steroids.

Animals↗