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PubMed1992

Growth hormone response to acute growth hormone releasing hormone administration in uraemic patients on haemodialysis.

To examine the response of growth hormone (GH) to growth hormone releasing factor (GHRF) in patients on haemodialysis, we performed the acute GHRF test (50 micrograms administered intravenously as a bolus) in 10 uraemic male patients on haemodialysis and eight normal controls. Each patient was tested before and after a haemodialysis session (at 08.30 and 12.30). Controls were tested on the same time schedule. At 08.30, patients had significantly greater basal and peak GH values (2.5 +/- 0.6 and 27.8 +/- 5.5 micrograms/l) than controls (0.68 +/- and 11.5 +/- 4 micrograms/l). After the haemodialysis session, basal and peak values declined significantly (P less than 0.01) in the uraemic group (0.5 +/- 0.03 and 3.1 +/- 1.1 micrograms/l), whereas the controls did not show such a change in the 12.30 test. Basal and intratest glycaemic values were comparable both before and after haemodialysis. After dialysis test results did not change either with the use of glucose-free dialysate or with bicarbonate buffer. Uraemic patients display a greater GH response to GHRF injection than normal subjects, and this response decreases after haemodialysis. The degree of reduction has no relationship with either glycaemia or the dialysate buffer. We suggest that other GH secretion regulating factors are altered by the haemodialysis procedure.

Adult↗
PubMed1997

Localization and quantification of binding sites for follicle-stimulating hormone, luteinizing hormone, growth hormone, and insulin-like growth factor I in sheep ovarian follicles.

In sheep, growth and development of ovarian follicles beyond 2 mm in diameter is acutely dependent on gonadotropin support. As a consequence, following hypophysectomy (HPX) or hypothalamic-pituitary stalk disconnection (HPD), growth of follicles beyond 2 mm is arrested and all follicles > 2 mm undergo atresia. Although administration of exogenous gonadotropins stimulates follicular growth and ovulation in HPD ewes, follicles in HPX ewes remain unresponsive unless growth hormone (GH) is also given. To determine whether the difference in follicular sensitivity to gonadotropins after HPD (gonadotropin sensitive) or HPX (gonadotropin insensitive) is related to the distribution and quantity of binding sites for FSH, LH, and/or insulin-like growth factor I (IGF-I), binding sites for these hormones were localized and quantified using topical autoradiography in healthy follicles from control (pituitary-intact), HPD, and HPX ewes. In addition, in situ hybridization was performed to localize mRNA for GH and FSH receptors. Irrespective of treatment, binding of FSH and mRNA for FSH receptor were greatest (p < 0.05) in the membrana granulosa; LH binding was greatest (p < 0.05) in the theca interna; and IGF-I binding was greatest (p < 0.05) in the theca externa. Although the relative number of binding sites for LH did not differ among treatments, those for FSH and IGF-I were lower (p < 0.05) in HPD and HPX ewes compared to controls. Attempts to quantify binding sites for GH were unsuccessful due to high nonspecific binding. However, mRNA for GH receptor was most abundant (p < 0.05) in the membrana granulosa and oocytes of small antral and preantral follicles. Compared to levels in controls and HPD ewes, the level of GH receptor mRNA was lower (p < 0.05) in follicles obtained from HPX ewes. On the basis of these data, failure of small antral follicles in HPX ewes to respond to exogenous gonadotropins is not due to a reduction in receptors for FSH, LH, or IGF-I. The observed reduction of mRNA for GH receptor in the membrana granulosa of follicles from HPX ewes provides evidence that GH may play an important role in early stages of folliculogenesis and that it is involved in the maintenance of sensitivity to gonadotropins.

Animals↗
PubMed1975

Hormonal profiles in anovulatory patients treated with gonadotropins and synthetic luteinizing hormone releasing hormone.

Ten patients with hypothalamic anovulation weretreated with a "retard" preparation of synthetic luteinizing hormone releasing hormone (LHRH) after an HMG stimulation in order to induce ovulation and pregnancy. Four of the patient ovulated after intramuscular administration of the LHRH preparation. This study suggests that is is possible to induce ovulation with LHRH in patients pretreated with HMG, and that LHRH has advantages over HCG since it does not induce hyperstimulation even in the presence of exagerated follicular growth. Nevertheless, the optimal conditions for the use and monitoring of LHRH treatment have yet to be clarified.

Adult↗
PubMed1991

Effects of pyridostigmine on spontaneous and growth hormone-releasing hormone stimulated growth hormone secretion in children on daily glucocorticoid therapy after liver transplantation.

OBJECTIVES: We aimed to investigate both nocturnal spontaneous and morning growth hormone (GH)-releasing hormone (GHRH)-induced GH secretion in children on daily glucocorticoid treatment after liver transplantation and to evaluate the effect of pyridostigmine (an acetylcholinesterase inhibitor thought to reduce hypothalamic somatostatin tone) on GH secretion in these patients. DESIGN: We performed a randomized, single-blind, cross-over study. PATIENTS: We studied three male and three female juvenile patients, within a year of orthotopic liver transplantation and under immunosuppressive glucocorticoid therapy (mean dose +/- SEM, 5.92 +/- 0.63 mg/day) and five normal children (four males, one female). MEASUREMENTS: Both nocturnal spontaneous and morning GHRH-induced GH secretion were evaluated after administration of placebo, 1 tablet p.o., or pyridostigmine, 2 mg/kg p.o. RESULTS: Spontaneous GH. Placebo: in liver transplanted children nocturnal GH secretion (mean GH level 10.8 +/- 2.0 mU/l) was not significantly different with respect to normal children (mean GH level 12.8 +/- 1.2 mU/l); pyridostigmine: nocturnal GH secretion was significantly increased as compared to placebo in subjects with liver transplantation but not in normal children. GHRH test. Placebo: liver transplanted patients showed a blunted GH response to GHRH with respect to normal children; pyridostigmine: the GH responses to GHRH (P less than 0.05) increased as compared to placebo and did not differ significantly in the two groups. CONCLUSIONS: Our data suggest a steroid-mediated increase in hypothalamic somatostatin tone in liver transplanted children.

Child↗
PubMed2005

Differential contribution of nitric oxide and cGMP to the stimulatory effects of growth hormone-releasing hormone and low-concentration somatostatin on growth hormone release from somatotrophs.

There is increasing evidence that nitric oxide (NO) produced by NO synthase (NOS), and their signalling partners, guanylyl cyclase and cGMP, play a relevant role in growth hormone (GH) secretion from somatotrophs. We previously demonstrated that both GH-releasing hormone (GHRH; 10(-8) M) and low concentrations of somatostatin (10(-15) M) stimulate pig GH release in vitro, whereas a high somatostatin concentration (10(-7) M) inhibits GHRH-induced GH secretion. To ascertain the possible contribution of the NOS-NO and guanylyl cyclase-cGMP routes to these responses, cultures of pituitary cells from prepubertal female pigs were treated (30 min) with GHRH (10(-8) M) or somatostatin (10(-7) or 10(-15) M) in the absence or presence of activators or blockers of key steps of these signalling cascades, and GH release was measured. Two distinct activators of NO route, SNAP (5x10(-4) M) or L-AME (10(-3) M), similarly stimulated GH release when applied alone (with this effect being blocked by 10(-7) M somatostatin), but did not alter the stimulatory effect of GHRH or 10(-15) M somatostatin. Conversely, two NO pathway inhibitors, NAME (10(-5) M) or haemoglobin (20 microg/ml) similarly blocked GHRH- or 10(-15) M somatostatin-stimulated GH release. 8-Br-cGMP (10(-8) to 10(-4) M) strongly stimulated GH release, suggesting that cGMP may function as a subsequent step in the NO pathway in this system. Interestingly, 10(-7) M somatostatin did not inhibit the stimulatory effect of 8-Br-cGMP. Moreover, although 8-Br-cGMP did not modify the effect of GHRH, it enhanced GH release stimulated by 10(-15) M somatostatin. Accordingly, a specific guanylyl cyclase inhibitor, LY-83, 583 (10(-5) M) did not alter 10(-15) M somatostatin-induced GH release, whereas it blocked GHRH-induced GH secretion. These results demonstrate for the first time that the NOS/NO signalling pathway contributes critically to the stimulatory effects of both GHRH and low-concentration somatostatin on GH release, and that, conversely, the subsequent guanylyl cyclase/cGMP step only mediates GHRH- and not low-concentration somatostatin-induced GH secretion from somatotrophs.

Animals↗
PubMed1987

Growth hormone releasing hormone in the assessment and long-term treatment of growth hormone deficiency.

The secretion of hGH after the administration of the analogue of growth hormone releasing hormone, GHRH (1-29)NH2, to 8 normal adults and 41 short children has been studied. The children were classified on the basis of their hGH response to insulin-induced hypoglycaemia; 28 had severe hGH deficiency (peak serum hGH less than 7 mIU/litre) and 13 had simple short stature (peak serum hGH greater than 15 mIU/litre). The hGH response to GHRH was similar in normal adults and short stature children, but significantly lower in the hGH deficient children. In 23 (82%) of the hGH deficient children the peak serum hGH in response to GHRH was greater than 7 mIU/litre (the maximum value seen during hypoglycaemia), and in 14 (50%) the peak serum hGH in response to GHRH was greater than 15 mIU/litre. This suggests that in the majority of hGH deficient children the defect in hGH secretion results from hypothalamic GHRH deficiency. The hGH responses of the short stature children to insulin-induced hypoglycaemia were mainly in the low range of normal, and the majority showed normal hGH responses to GHRH. Eighteen prepubertal children with definite hGH deficiency have been treated for 3-18 months with twice daily, subcutaneous injections of GHRH. This has promoted linear growth in 12 children, of whom 8 showed an increment in height velocity of 2-11 cm/year. GHRH provides a valuable method for the assessment of hGH secretion, but by itself it cannot be used to establish deficient hGH secretion; this requires a stimulation test that promotes hypothalamic GHRH secretion, such as insulin-induced hypoglycaemia. GHRH is a practical alternative therapy to hGH for some hGH-deficient children.

Adult↗
PubMed1989

Growth hormone response to overnight growth hormone-releasing hormone infusion and oral pyridostigmine in children with short stature.

The development of a long-acting or depot preparation of growth hormone-releasing hormone (GHRH) may have many advantages over conventional treatment (with GH) of GH-deficient children. Pyridostigmine, an acetylcholinesterase inhibitor, has been shown to augment basal GH secretion and the GH response to GHRH in short children. It may thus provide adjuvant therapy to depot GHRH. The GH response to a nocturnal subcutaneous infusion of GHRH (1-29)NH2 in doses of 5 and 10 micrograms/kg/hour was investigated in five short, slowly growing children. The effect of oral pyridostigmine 60 mg on nocturnal GH secretion and the GH response to a nocturnal infusion was also examined. The subcutaneous infusion of GHRH augmented pulsatile GH release in all five children. There was a dose-related response to subcutaneous GHRH for the GH area under the curve and mean GH pulse amplitude, but no change in the number of pulses. There was a significant rise in the mean baseline GH concentration during the GHRH infusion compared with placebo. Pyridostigmine had no effect on either basal or stimulated GH secretion.

Child↗
PubMed1998

Growth hormone releasing hormone expression during postnatal development in growth hormone-deficient Ames dwarf mice: mRNA in situ hybridization.

Several genetic mutations in mice and rats that produce lifelong growth hormone (GH) deficiency result in overexpression of GH-releasing hormone (GHRH) mRNA in hypothalamic arcuate nucleus neurons. In order to examine the development of this condition, GHRH mRNA expression was quantified in Ames dwarf (df/df) and normal (DF/?) mice at 1 (day of birth), 3, 7, 14, 21 and 60 postnatal days (d) following in situ hybridization. Total mRNA was assessed using computer-assisted densitometry after X-ray film autoradiography, and mRNA expression per neuron was quantified by counts of grains per cell after emulsion autoradiography. Total GHRH mRNA was the same in dwarf and normal mice at 1, 3 and 7d. GHRH mRNA in dwarfs increased at 14d to 240% of that in DF/? (p < 0.005); the percentage overexpression in dwarf mice remained >/=200% through 60d, although total GHRH mRNA increased in both dwarfs and normals during this period. GHRH mRNA per neuron was the same in normal and dwarf mice at 1d, then increased in dwarfs to 190% of that in normals at 3d (p < 0.05), and rose to 300% of normal levels by 7d and beyond (p < 0. 005). There was no sexual dimorphism in expression by either measure in normal or dwarf mice. These results indicate that an increase in GHRH mRNA in Ames dwarf mice is first detectable at 3d, a period of approximately 7d after the failure to initiate GH production, which occurs normally at embryonic day 17.5. The onset of GHRH overexpression occurs earlier than the decline of either hypophysiotropic somatostatin or dopamine in Ames dwarf mice. This difference may be due to the stimulatory action of GHRH, as opposed to the inhibitory effects of factors examined previously.

Animals↗
PubMed2006

Regulation of 5'-promoter activity of the rat growth hormone and growth hormone-releasing hormone receptor genes in the MtT/S and MtT/E cells.

The MtT/E and MtT/S cells have been established from a mammotrophic pituitary tumor, and postulated to be progenitor and premature growth hormone (GH) cells, respectively. The difference in the regulation of GH and GH-releasing hormone (GHRH) receptor gene transcription in relation to the developmental stage of GH cells were examined in these two cell lines. In MtT/S cells, triiodothyronine (T3), all-trans retinoic acid (RA) and 9-cis retinoic acid (9cRA) stimulated GH promoter activity but dexamethasone (DEX) did not. On the other hand, DEX stimulated GHRH-receptor promoter alone. T3, RA and 9cRA showed little effect alone but each of them augmented the effect of DEX when used together with DEX. In MtT/E cells, DEX, RA and 9cRA showed similar effect as observed in MtT/S cells on both GH and GHRH-receptor promoter activity. However, T3 neither stimulated GH promoter activity nor augmented the DEX-induced GHRH-receptor gene transcription in MtT/E cells. RT-PCR analyses revealed that both cell types expressed TRalpha1, TRbeta1 and TRalpha2, but expression of TRbeta2, a pituitary specific isoform of TR, was only detected in MtT/S cells. However, the deficiency of TRbeta2 for its own sake does not appear to be a reason why T3 action was not observed in MtT/E cells, because co-transfection of expression plasmids for TRbeta2 and RXRalpha failed in conferring on the cells an ability to respond to T3 by increased GH or GHRH-receptor promoter activity. These results suggest that the acquisition of mechanisms responsible for the regulation of GH or GHRH-receptor transcription by T3 may be involved in the process of functional development of GH cells.

Animals↗
PubMed1980

Growth hormone response to thyrotropin-releasing hormone and gonadotropin-releasing hormone stimulation in heroin addicts.

Previous endocrine investigations have demonstrated the presence of multiple impairments of pituitary-target gland function in heroin addicts suggesting a possible hypothalamic involvement. Since the response of the pituitary to nonspecific stimuli is considered an expression of hypothalamic dysfunction, indicating a disconnection between the central nervous system and the anterior pituitary, we thought it worthwhile to study the GH response to stimulation with thyrotropin-releasing hormone (TRH) or gonadotropin-releasing hormone (GnRH) in heroin addicts. 23 male heroin addicts, aged 18-40 years, with histories of addiction to heroin alone from 8 months to 4 years, and daily i.v. heroin intakes between 200 and 2,500 mg of the drug (containing 18% pure heroin) were studied. 8 patients received TRH 500 micrograms, GnRH 150 micrograms and 5 saline only, intravenously, and GH levels were assayed radioimmunologically in bloods taken 30 min before, at the moment of stimulation and 15, 30, 60, 90 and 120 min thereafter. The results show normal base GH levels. Stimulation with TRH and GnRH induced marked GH hypersecretion in 8 of the 18 patients examined. These results suggest that the hypothalamo-pituitary function may be impaired in heroin addiction.

Adolescent↗
PubMedDate not supplied

Cholinergic modulation of growth hormone-releasing hormone effects on growth hormone secretion in dementia.

An impairment of cholinergic and somatostatinergic neurotransmission have been reported in dementia. Both acetylcholine and somatostatin are involved in the regulation of growth hormone (GH) secretion. The effects of GH-releasing hormone (GHRH) 1-44 on GH release have been studied before and after the pretreatment with pyridostigmine or pirenzepine in subjects with senile dementia of the Alzheimer type, multi-infarct dementia and mixed dementia. The data have been compared with those obtained in an age-matched healthy control group. The GH response to GHRH is similar in the patients and in the controls, though the peak occurrence is significantly delayed in dementia. The cholinesterase inhibitor pyridostigmine enhances significantly the GH response to GHRH in both groups. The responses obtained in demented subjects are significantly larger than those found in the controls. Pirenzepine, a muscarinic receptor blocker, inhibits the GHRH effect on GH secretion in both groups. The findings may be interpreted in terms of an underlying impairment of the hypothalamic cholinergic neurotransmission, with an acetylcholine receptor supersensitivity that becomes apparent when the cholinergic tonus is enhanced by the inhibition of cholinesterase by pyridostigmine. No significant differences, due to the type of dementia, have been observed.

Acetylcholine↗
PubMed1987

Dopaminergic and cholinergic influences on the growth hormone response to growth hormone-releasing hormone in man.

It is well established that compounds that modify dopaminergic and cholinergic activity in man may induce changes in circulating growth hormone (GH). We have, therefore, investigated the effect of a dopamine agonist, bromocriptine, and a dopamine antagonist, domperidone, as well as a muscarinic cholinergic antagonist, pirenzepine, on the GH response to an analogue of GH-releasing hormone (GHRH) in normal male subjects. GHRH(1-29)NH2 induced a rise in serum GH that was augmented by bromocriptine, antagonized by pirenzepine, but was unaltered by domperidone. As this dose of GHRH(1-29) NH2 has been shown to be maximally stimulatory to GH release, it is suggested that there are dopamine stimulatory and cholinergic inhibitory receptors to GH release independent of GHRH in man.

Adrenergic Fibers↗
PubMed1988

Depending on the time of administration, dexamethasone potentiates or blocks growth hormone-releasing hormone-induced growth hormone release in man.

In humans, corticoids suppress growth hormone (GH) secretion elicited by a variety of stimuli, while in vitro they potentiate GH release. To further study this problem, the effect of two doses of dexamethasone on GH secretion elicited by GH-releasing hormone (GHRH) in 6 normal volunteers was studied. Each subject underwent three tests, on 3 separate days with GHRH 1-29 (1 microgram/kg i.v. at 12.00 h). On the control day, only GHRH was given, on the second day dexamethasone 4 mg i.v. was administered at 09.00 h (3 h before GHRH) and on the third day dexamethasone 8 mg p.o. was given 12 h before GHRH (at 00.00 h). The GHRH-induced GH peak was 9.9 +/- 2.0 ng/ml, while 4 mg dexamethasone significantly (p less than 0.05) potentiated GH secretion elicited by GHRH (29.2 +/- 5.7 ng/ml). When dexamethasone 8 mg was given 12 h before, GHRH-induced GH secretion was completely blocked (3.0 +/- 1.1 ng/ml) (p less than 0.05). These results indicate that corticoids have two different actions: an acute potentiating activity on GHRH, and a delayed blocking action on GHRH-induced GH secretion.

Adult↗
PubMed1988

Growth hormone releasing hormone induced release of growth hormone in aging male rats: dependence on pharmacological manipulation and endogenous somatostatin release.

These studies were designed to assess whether a decline in pituitary response to growth hormone-releasing factor (GRF) contributes to the decline in amplitude of growth hormone (GH) pulses with age. Atrial cannulated young (3-4 months), middle-aged (12-14 months) and old (20-22 months) Fischer 344 male rats were anesthetized with pentobarbital to suppress pulsatile release of GH. One hour later, animals were injected with hpGRF(1-44) (10 micrograms/kg) and blood samples were removed at 0, 5, 10, 20, 40 and 80 min. Animals were then passively immunized with somatostatin antiserum and hpGRF(1-44) was reinjected. Samples were removed at the time intervals previously described. In response to 10 micrograms/kg GRF, plasma GH in young and middle-aged animals increased to 921 +/- 105 and 866 +/- 126 ng/ml, respectively, at 10 min and declined. In old animals, GH concentrations only increased to 654 +/- 80 ng/ml (p less than 0.05 compared to young rats). This represents a 28% reduction in the peak GH response to GRF. Despite passive immunization with somatostatin antiserum, the peak GH response to a second injection of GRF was diminished in all age-groups. However, integration of the area under the response curve indicated that GH secretion was similar in young and old animals during the 80-min sampling period after somatostatin antiserum. In another study, diethyldithiocarbamate (DDC; 250 mg/kg, i.v.), a dopamine-beta-hydroxylase inhibitor, was used to inhibit pulsatile GH release. One hour later, animals were injected with hpGRF(1-44) (50 micrograms/kg, i.v.) and blood samples were removed as previously described.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Pharmacodynamics of gonadotropin-releasing hormone. 1. Effects of gonadotropin-releasing hormone pulse contour on pituitary luteinizing hormone secretion in vivo in sheep.

The gonadotropin-releasing hormone (GnRH) waveform arrives at the pituitary gonadotropes via the pituitary portal blood and provides the immediate suprapituitary stimulus to luteinizing hormone (LH) secretion. Despite their importance, nature and influence of the physiological GnRH waveform in vivo have been difficult to study. Recent pharmacological and in vitro studies have suggested the potential importance of the wave contour as a specific and independent factor in the pharmacodynamic effects of GnRH on pituitary gonadotrope LH secretion in vivo, and it has been hypothesized that the steepness of the rising edge of the GnRH wave contour is a specific determinant of pituitary LH secretion. In order to investigate the pharmacodynamic influence of GnRH pulse wave contour on pituitary LH secretion in vivo, variations in plasma LH responses to alterations in GnRH wave contour were measured in chronic ovariectomized, hypothalamopituitary-disconnected sheep undergoing physiological pulsatile GnRH maintenance regimen at a fixed dose (250 ng/pulse) and frequency (interpulse interval 120 min). Variable wave contours were then generated by administration of the same total GnRH pulse dose over various lengths of time from near-instantaneous bolus to increasing lengths of constant-rate infusion time up to 8 min. This model allowed specific examination of pulse wave contour in the absence of concurrent changes in endogenous GnRH or sex steroid secretion and holding constant GnRH pulse dose, frequency, and route of administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Growth hormone responses to growth hormone-releasing hormone in Hand-Schüller-Christian Disease.

Bolus doses of GH-releasing hormone (GHRH), 1 microgram/kg i.v., were given to two groups of adult patients with growth hormone deficiency (GHD): 9 with Hand-Schüller-Christian disease (HSCD, presumed hypothalamic GHD) and 9 with idiopathic GHD (IGHD, etiology unknown). Six patients in each group were then given further GHRH doses daily for 5 days, and the GH responses to GHRH were measured over 3 h on day 1 and day 5. Plasma levels of insulin-like growth factor-I (IGF-I) were measured twice daily on days 1 and 5 during GHRH treatment. All patients with HSCD had measurable GH responses to the first dose of GHRH, with a mean peak response of 6.4 +/- 2.1 ng/ml (mean +/- SE). Only 5 of 9 patients with IGHD had GH responses above the detection limits of the assay; their mean peak response, 1.3 +/- 0.2 ng/ml, was significantly lower than the GH responses of the HSCD patients (p less than 0.05). Responses in both groups of patients were lower than those previously observed in normal adult men (35 +/- 8 ng/ml; p less than 0.01). Five days of daily stimulation with GHRH significantly (p less than 0.01) increased the GH response in both groups of patients. The rise was greater in patients with HSCD than with IGHD (HSCD, 5.1 +/- 2.5 ng/ml on day 1, vs. 12.0 +/- 6.8 ng/ml on day 5; IGHD, 1.4 +/- 0.3 ng/ml vs. 2.9 +/- 0.6 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effect of hypophysectomy and growth hormone administration on hypothalamic growth hormone-releasing hormone and somatostatin content: relationship to age-related growth rate.

The purpose of these studies was to evaluate the effect of age-related differences in growth rate on the hypothalamic content of growth hormone-releasing factor (GHRH) and somatostatin (SS) and on the short loop feedback regulation of GHRH and SS. Percent weight gain, GHRH content, and SS content in control adolescent (8 weeks) and adult rats (6 months) were compared in normal rats administered supraphysiologic amounts of rat growth hormone (rGH) or in hypophysectomized rats receiving thyroxine and corticosterone with or without physiologic rGH replacement. In control adolescent rats, the rate of weight gain was 5-fold higher than in adult rats. GHRH content was higher in adolescent rats, while SS content was lower. After the administration of supraphysiologic amounts of rGH, GHRH content increased in adolescent rats but did not change in adult rats. SS content was unchanged in either age group. Following hypophysectomy GHRH content declined similarly in both groups, whereas the decrease in SS content was greater in adolescent rats. With replacement rGH, weight gain was restored, GHRH content increased but not fully to control, and SS content did not change. The ratio of SS content to GHRH content (SS/GHRH) was higher in control adult rats than in adolescent rats. SS/GHRH increased following hypophysectomy and returned to control values by rGH replacement. We conclude that age-related differences in growth rate are accompanied by appropriate changes in SS/GHRH and that SS and GHRH are regulated by short loop feedback at both ages with increased responses in adolescent rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

Role of hypothalamic factors (growth-hormone-releasing hormone and gamma-aminobutyric acid) in the regulation of growth hormone secretion in the neonatal and adult rat.

N-methyl aspartic acid (NMA) was without effect on the pituitary growth hormone (GH) secretion of adult and neonatal rats in vitro. Administration of NMA resulted in a rapid rise of plasma GH levels in intact but not in arcuate-nucleus-lesioned adult rats, indicating that NMA stimulated GH-releasing hormone (GRH) secretion. In 2-day-old rats, both NMA and gamma-aminobutyric acid (GABA) elevated plasma GH levels in a dose-related fashion; GRH administration was without effect. The elevation of plasma GH levels after NMA injection was reduced by administering an antibody to GRH. These results indicate that GH secretion is partly regulated by endogenous GRH in the newborn rat but that the elevation of plasma GH levels after GABA is not mediated by GRH. The high plasma GH levels seen in the newborn rat may result from the independent action of GABA and GRH but the effect of other factors cannot be excluded either.

Aging↗