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PubMed1996

Circulating maternal corticotropin-releasing hormone and gonadotropin-releasing hormone in normal and abnormal pregnancies.

OBJECTIVE: Corticotropin-releasing hormone and gonadotropin-releasing hormone are produced by the human placenta and have been measured in the maternal circulation during pregnancy. Our objective was to determine concentrations of these substances in maternal plasma throughout normal pregnancies and in early pregnancy loss. STUDY DESIGN: Fifty-one pregnant women were followed up prospectively and plasma samples were drawn at 8, 10, 12, 14, 16, 28, and 36 weeks' gestation and during labor. Specific and sensitive radioimmunoassays were used to determine corticotropin-releasing hormone and gonadotropin-releasing hormone concentrations in these samples. RESULTS: Blood samples were drawn at all time points and outcome data were available from 33 women who completed their pregnancies at term without complications. In this normal group circulating corticotropin-releasing hormone concentrations increased from low or undetectable concentrations at 8 weeks (< or = 23.2 +/- 1.3 pg/ml, mean +/- SEM) to measurable values at 16 weeks (34.3 +/- 2.2 pg/ml). Thereafter there was a significant increase to 1294 +/- 113 pg/ml in labor. Gonadotropin-releasing hormone demonstrated a trimodal distribution, increasing significantly from 8 to 14 weeks, decreasing at 16 weeks, and increasing again by term. The ratio of corticotropin-releasing hormone to gonadotropin-releasing hormone in the normal group demonstrated a 30-fold increase from 8 weeks to term. In eight cases of early pregnancy loss corticotropin-releasing hormone and gonadotropin-releasing hormone concentrations were not significantly different from those of the normal group in early pregnancy. In two cases of premature delivery gonadotropin-releasing hormone concentrations and ratios were within the normal range; corticotropin-releasing hormone levels were normal in both cases of premature delivery. CONCLUSION: In this study we determined maternal concentrations of corticotropin-releasing hormone and gonadotropin-releasing hormone in normal pregnancies and in labor at term. Neither maternal concentrations of corticotropin-releasing hormone nor gonadotropin-releasing hormone were useful in identifying pregnant women at risk for early pregnancy loss.

Abortion, Spontaneous↗
PubMed2001

A regulator of G protein signaling, RGS3, inhibits gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) secretion.

BACKGROUND: Luteinizing hormone secreted by the anterior pituitary gland regulates gonadal function. Luteinizing hormone secretion is regulated both by alterations in gonadotrope responsiveness to hypothalamic gonadotropin releasing hormone and by alterations in gonadotropin releasing hormone secretion. The mechanisms that determine gonadotrope responsiveness are unknown but may involve regulators of G protein signaling (RGSs). These proteins act by antagonizing or abbreviating interaction of Galpha proteins with effectors such as phospholipase Cbeta. Previously, we reported that gonadotropin releasing hormone-stimulated second messenger inositol trisphosphate production was inhibited when RGS3 and gonadotropin releasing hormone receptor cDNAs were co-transfected into the COS cell line. Here, we present evidence for RGS3 inhibition of gonadotropin releasing hormone-induced luteinizing hormone secretion from cultured rat pituitary cells. RESULTS: A truncated version of RGS3 (RGS3T = RGS3 314-519) inhibited gonadotropin releasing hormone-stimulated inositol trisphosphate production more potently than did RSG3 in gonadotropin releasing hormone receptor-bearing COS cells. An RSG3/glutathione-S-transferase fusion protein bound more 35S-Gqalpha than any other member of the G protein family tested. Adenoviral-mediated RGS3 gene transfer in pituitary gonadotropes inhibited gonadotropin releasing hormone-stimulated luteinizing hormone secretion in a dose-related fashion. Adeno-RGS3 also inhibited gonadotropin releasing hormone stimulated 3H-inositol phosphate accumulation, consistent with a molecular site of action at the Gqalpha protein. CONCLUSIONS: RGS3 inhibits gonadotropin releasing hormone-stimulated second messenger production (inositol trisphosphate) as well as luteinizing hormone secretion from rat pituitary gonadotropes apparently by binding and suppressing the transduction properties of Gqalpha protein function. A version of RGS3 that is amino-terminally truncated is even more potent than intact RGS3 at inhibiting gonadotropin releasing hormone-stimulated inositol trisphosphate production.

Animals↗
PubMed1986

Effect of chronic growth hormone treatment on responses to epinephrine and thyrotropin-releasing hormone in lactating cows.

Bovine growth hormone was administered to four Holstein cows (late lactation) in a Latin square. Treatments were 1) control, subcutaneous injection of placebo, 2) subcutaneous injection of 25 IU growth hormone on alternate days, 3) daily subcutaneous injection of 25 IU growth hormone, and 4) continuous subcutaneous infusion of 25 IU/d growth hormone. Intravenous challenges of epinephrine and thyrotropin-releasing hormone were administered separately on the 1st d after a 12-d interval of growth hormone treatment. Baseline concentrations of nonesterified fatty acids in plasma were not affected by growth hormone treatment. However, release of nonesterified fatty acids to epinephrine challenge was positively related to amount of growth hormone in plasma during treatment and was correlated with milk fat yield and milk energy secretion. Growth hormone release following thyrotropin-releasing hormone was negatively related to amount of growth hormone in plasma during treatment. Release of prolactin to thyrotropin-releasing hormone challenge was not related to average daily dose of exogenous growth hormone. The galactopoeitic action of growth hormone may be partly attributable to its effects on responsiveness of adipose tissue to a lipolytic stimulus but apparently is not associated with changes of pituitary sensitivity to thyrotropin-releasing hormone. Results are consistent with growth hormone functioning as a homeorhetic control of nutrient partitioning.

Animals↗
PubMed1998

Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones.

To study the hormonal perturbations in FMS patients we injected sixteen FMS patients and seventeen controls a cocktail of the hypothalamic releasing hormones: Corticotropin-releasing hormone (CRH), Thyrotropin-releasing hormone (TRH), Growth hormone-releasing hormone (GHRH), and Luteinizing hormone-releasing hormone (LHRH) and observed the hormonal secretion pattern of the pituitary together with the hormones of the peripheral endocrine glands. We found in FMS patients elevated basal values of ACTH and cortisol, lowered basal values of insulin-like growth factor I (IGF-I) and of triiodothyronine (T3), elevated basal values of follicle-stimulating hormone (FSH) and lowered basal values of estrogen. Following injection of the four releasing-hormones, we found in FMS patients an augmented response of ACTH, a blunted response of TSH, while the prolactin response was exaggerated. The effects of LHRH stimulation were investigated in six FMS patients and six controls and disclosed a significantly blunted response of LH in FMS. We explain the deviations of hormonal secretion in FMS patients as being caused by chronic stress, which, after being perceived and processed by the central nervous system (CNS), activates hypothalamic CRH neurons. CRH, on the one hand, activates the pituitary-adrenal axis, but also stimulates at the hypothalamic level somatostatin secretion which, in turn, causes inhibition of GH and TSH at the pituitary level. The suppression of gonadal function may also be attributed to elevated CRH by its ability to inhibit hypothalamic LHRH release, although it could act also directly on the ovary by inhibiting FSH-stimulated estrogen production. We conclude that the observed pattern of hormonal deviations in FMS patients is a CNS adjustment to chronic pain and stress, constitutes a specific entity of FMS, and is primarily evoked by activated CRH neurons.

Adrenocorticotropic Hormone↗
PubMed1992

Effect of cholinergic tone on growth hormone-releasing hormone-induced secretion of growth hormone in normal aging.

Aging is associated with an impairment in the GH response to GHRH and to several other stimuli of GH secretion. We evaluated the effect of pyridostigmine (PD) or placebo pretreatment (Protocol A: placebo or 120 mg PD orally at 8 a.m.; Protocol B: placebo or 60 mg PD twice orally at 9 p.m. and 7 a.m.) on GH responsiveness to GHRH (1 micrograms/kg BW bolus i.v. at 9 a.m.) in 15 normal elderly males (65-92 years) and in 14 normal young adults (20-37 years). GH response to GHRH was significantly reduced in elderly subjects compared to young adults (p < 0.05). PD (Protocol A) increased GH release in both elderly and young subjects. In elderly men, PD enhanced GH response to GHRH. The phenomenon was more evident when PD was administered according to Protocol B (p < 0.01). The area under the curve of GH was significantly greater after PD plus GHRH than it was after placebo plus GHRH (p < 0.01). In young adults, PD induced an increase in GH responsiveness to GHRH when administered according to Protocol A (p < 0.05) but not Protocol B. Both GH peak and AUC of GH after PD plus GHRH (Protocols A and B) in elderly subjects were not significantly different from the same parameters found in young subjects after placebo plus GHRH. Our data confirm that pituitary somatotrophin responsiveness to GHRH in man changes with aging. PD restores GH responsiveness to GHRH in elderly subjects. The effect of PD on GH secretion suggests that cholinergic mechanisms may be involved in GH control in normal aging.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Role of growth hormone-releasing hormone on pentagastrin-induced growth hormone release in normal subjects.

In order to investigate the mechanisms by which gastrin cause GH release in humans we measured the GH response to pentagastrin alone (1.5 micrograms/kg/hour from 120 to 210 min) and following pretreatment with GHRH (GHRH 1-29,250 micrograms, iv at 0 min) in normal male subjects. Prior GHRH administration abolished the GH response to the second bolus of GHRH (1 micrograms/kg) administered two hours later. Pentagastrin infusion induced a rise in GH levels maximal at 60 min (9.1 + 0.6 ng/ml, mean + SE), but this rise was abolished by pretreatment with GHRH. Finally, we found that gastrin did not modify basal GH release or GH responses to GHRH by rat anterior pituitary cells in monolayer culture. Taken together, these data suggest that gastrin regulates GH secretion by acting at hypothalamic level.

Adult↗
PubMed1991

Sex differences in growth hormone response to growth hormone-releasing hormone.

The aim of the present study was to ascertain whether sex differences exist in GH response to GHRH, and the influence that menstrual cycle have on this response. A GHRH test was performed on nine healthy men and ten women on days one and twelve of the menstrual cycle. Basal GH levels, (mean +/- SE) (7.98 +/- 3.09 ng/ml in women and 0.13 +/- 0.07 ng/ml in men, p less than 0.05) as well as maximal GH response (40.17 +/- 11.96 ng/ml in women and 9.63 +/- 2.32 ng/ml in males, p less than 0.01) were significantly higher in women than in men. In spite of a significant increase in estradiol levels during the menstrual cycle (75.88 +/- 2.48 pg/ml on day one and 198.40 +/- 28.65 pg/ml on day twelve, p less than 0.01) neither basal plasma GH levels, nor GH response to GHRH were significantly different. In conclusion, these results confirm that GH response to GHRH is higher in women than in men, and that this difference is not modified during the first phase of the menstrual cycle.

Adult↗
PubMed1991

Follicle stimulating hormone-secreting pituitary adenoma: inappropriate secretion and effect of pulsatile luteinizing hormone releasing hormone analogue (buserelin) administration.

A patient with an FSH secreting pituitary adenoma is reported. Elevated FSH and serum free alpha-subunit (SU) with low levels of LH and testosterone (T) were found. Immunostaining showed the presence of alpha-SU, FSH-beta and LH-beta subunits. LHRH analogue (buserelin) was administered in a pulsatile manner, by portable computerized infusion pump sc for ten days. During the first 24 h of treatment FSH, LH (p less than 0.001) and T (p less than 0.01) rose significantly. Ten days later, the expected desensitization phenomenon did not occur, but further increases of T (8.4 +/- 2.6, mean +/- SD, vs 17.4 +/- 4.1 nmol/l, p less than 0.001) and FSH (58.9 +/- 9.6 vs 70.7 +/- 3.8 mlU/ml, p less than 0.001) were registered. LH decreased (12.5 +/- 2.4 vs 7.1 +/- 0.6 mlU/ml, p less than 0.001) at day 10, but remained higher than basal level (5.0 +/- 0.6, p less than 0.001). Free alpha-SU also rose (2.8 +/- 0.4 vs 4.4 +/- 1.7 mlU/ml, p less than 0.001) after ten days of treatment. The chronic stimulatory effect of analogue on LH with a lack of desensitization suggests tumorous secretion despite a partially preserved negative feedback of testosterone. Low basal LH levels, in some patients with FSH secreting tumors may not be due to tumor mass effect, but rather may be the consequence of altered LH production and/or secretion by the tumor. Although buserelin may not have a therapeutic effect, it is of use in differential diagnosis of hypergonadotropinemia.

Adenoma, Chromophobe↗
PubMed1993

Galanin infusion partially restores the blunted growth hormone responses to repeated growth hormone releasing hormone stimuli in normal adults.

In order to understand the role exerted by the endogenous somatostatinergic tone in the blunting of GH responsiveness to repeated GHRH administration, we evaluated GH responses to the second GHRH bolus during a simultaneous infusion of galanin, which has been reported to inhibit the endogenous somatostatin release. Seven normal adults (3M/4F, age range 19-28 yr), admitted to the study after giving informed consent, were tested on three occasions, with a) two consecutive 1 micrograms/kg iv GHRH boluses administered at 0 min and 120 min, b) one GHRH bolus at 0 min followed by an infusion of 10 micrograms/kg bw galanin (diluted in 40 ml 0.9% NaCl) between 100 min and 140 min and c) two consecutive GHRH boluses (same dose and temporization of administration of test a) associated with a galanin infusion from 100 min to 140 min. GH responses were evaluated as the net incremental area under the curve (GH nAUC/h); all data were expressed as mean +/- SE. GH responses to the first GHRH bolus were similar in the three tests (mean GH nAUC, test A 990 +/- 80, test B: 1006 +/- 112, test C: 1077 +/- 80 ng/ml/h). In test A the second GHRH bolus was unable to sustain GH elevated levels (mean GH nAUC: 32 +/- 12 ng/ml/h vs first GHRH: 990 +/- 80 ng/ml/h, p < 0.0001). Similarly, in test B galanin infusion alone was unable to determine a clear GH rise (mean GH nAUC: -25 +/- 16 vs first GHRH: 1006 +/- 112 ng/ml/h, p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Low doses of either intravenously or orally administered arginine are able to enhance growth hormone response to growth hormone releasing hormone in elderly subjects.

Reportedly, the responsiveness of somatotrope cells to GHRH is reduced in elderly humans but it is totally restored by arginine (ARG) which likely acts by inhibiting hypothalamic release of somatostatin. As this effect was observed after infusion of high doses of the amino acid, in this study, we compared the effect of iv administration of 30, 10 and 5 g ARG(group A, B and C, respectively) as well as oral administration of 8 g ARG(group D) on the GH response to 1 microgram/kg i.v.GHRH in 27 healthy elderly subjects (11 M and 16 F, age 70-86 yr, BMI 21-25 kg/m2). In group A (n = 7) 30 g i.v. ARG strikingly enhanced the GHRH-induced GH rise (peak, mean +/- SE: 41.5 +/- 4.4 vs 11.7 +/- 5.3 micrograms/L, p < 0.05). Similarly, in group B (n = 6) and D (n = 7) 10 g i.v. and 8 g oral ARG enhanced the GH response to GHRH (20.9 +/- 4.7 vs 8.3 +/- 2.8 micrograms/L, p < 0.03 and 31.0 +/- 5.3 vs 11.4 +/- 3.4 micrograms/L, p < 0.03, respectively). In contrast, in group C (n = 7) 5 g i.v. ARG failed to modify the GHRH-induced GH rise (6.0 +/- 1.6 vs 3.5 +/- 0.9 micrograms/L). The GH responses to GHRH alone did not significantly differ amongst groups; the GH responses to GHRH and ARG were not significantly different among groups A, B and D and were greater than the GH response in group C. These results show that the GH response to GHRH in elderly subjects is enhanced even by low iv doses of arginine and by the orally administered amino acid, the lowest effective dose being 8 g. Moreover, they imply that the combined administration of GHRH and arginine may be a useful approach to restore the impaired function of the GH-IGF axis in aging.

Administration, Oral↗
PubMed1995

Interaction of salbutamol and galanin on both basal and growth hormone releasing hormone-stimulated growth hormone secretion in humans.

Beta adrenergic receptors mediate the inhibitory influence of catecholamines on GH secretion in man, likely via stimulation of hypothalamic somatostatin release. To further clarify the role of beta adrenergic receptors in the neural control of GH secretion, in 7 normal females (age 21-27 yr) we studied the interaction of salbutamol (SAL 0.08 mg/kg orally), a beta 2-adrenergic agonist, with GHRH (1 microgram/kg i.v.) and/or galanin (GAL 15 micrograms/kg i.v.), a neuropeptide endowed with a GH-releasing effect which is likely mediated by concomitant stimulation of GHRH- and inhibition of somatostatin-secreting neurons. SAL inhibited the GH response to GHRH (AUC: 282.6 +/- 102.7 vs 1083.6 +/- 176.5 micrograms/l/h, p < 0.05) and, although not significantly, that to GAL (263.9 +/- 103.7 vs 418.4 +/- 70.4 micrograms/l/h). GAL enhanced the GHRH-induced GH rise (2129.5 +/- 362.2 micrograms/l/h, p < 0.05) but SAL pretreatment inhibited this effect (1249.8 +/- 257.1 micrograms/l/h, p < 0.02) so that the GH response to the combined administration of GHRH, GAL and SAL overlapped with that to the neurohormone alone. In conclusion, our results show that the inhibitory influence of beta adrenergic activation on GH secretion overrides the stimulatory one of galanin. They strengthen the view that in man beta-adrenergic receptors and galanin modulate GH secretion having opposite influences aimed to balance the function of the GH-IGF-I axis.

Adrenergic alpha-Agonists↗
PubMed1992

Growth hormone release during insulin tolerance, clonidine, arginine and growth hormone releasing hormone tests in short normal children and adolescents.

This study was retrospectively performed in 574 short normal children and adolescents [328 underwent insulin tolerance test (ITT), 34 clonidine test (CLON), 64 arginine test (ARG), 19 GHRH test, 52 ITT+CLON, 30 GHRH+CLON, and 47 ITT+CLON+GHRH) in order to evaluate the effect of pubertal stage on GH response to different tests and to identify the most likely mechanism of action of different stimuli. GH peak was higher during GHRH than in all other tests. Sex or start of pubertal development did not cause any GH peak difference. Low-responder (GH peak less than 10 ng/ml) percentages were similar (ITT = 13.5%, CLON = 13.4%, ARG = 13.2%, GHRH = 10.6%) also when the subjects were divided according to sex and pubertal development. ITT+CLON showed discordant results in 42/99 subjects (30/42 = 71.4% were low-responders to ITT and 12/42 = 28.6% to CLON). GH peak appeared earlier during GHRH (85% less than 45 min) and later during CLON (78%: 60-120 min) than during all other tests; GH peak during ITT showed a wide variability of time. Negative correlations were found between GH peak during GHRH and chronological age, height and bone age and during CLON and chronological age. In conclusion our data show that these tests have similar GH secretagogue reliability.

Adolescent↗
PubMedDate not supplied

Low dose orally administered arginine is able to enhance both basal and growth hormone-releasing hormone-induced growth hormone secretion in normal short children.

Aim of this study was to verify whether arginine (ARG), which likely inhibits hypothalamic somatostatin release, has an enhancing effect on the GHRH-induced GH rise, even when administered orally at low dose. To this goal we studied the effects of 4 g orally administered ARG, either hydrochloride (ARG-H) or aspartate (ARG-A), on both basal and GHRH (1 microgram/Kg i.v.)-stimulated GH secretion in 31 children with familial short stature (11 males and 20 females, aged 5.5-13.8 yr, pubertal stage I-III, and compared the results with those of i.v. infusion of 0.5 g/kg ARG-H. Oral ARG-H (Group A, n = 11) induced a significant increase of basal GH levels (4.2 +/- 1.3 vs 1.0 +/- 0.4 micrograms/L, p < 0.02) and enhanced the GH response to GHRH (41.1 +/- 8.6 vs 25.3 +/- 6.7 micrograms/L, p < 0.02). Oral ARG-A (Group B, n = 10) induced a slight, but not statistically significant increase in serum GH levels (3.4 +/- 1.5 vs 1.0 +/- 0.3 micrograms/L) and enhanced the GHRH-induced GH rise (49.7 +/- 9.8 vs 26.1 +/- 8.4 micrograms/L, p < 0.05). Intravenous ARG-H (Group C, n = 10) stimulated basal GH levels (6.2 +/- 1.2 vs 1.2 +/- 0.3 micrograms/L, p < 0.005) and increased the GHRH-induced GH rise (46.7 +/- 5.0 vs 17.1 +/- 2.3 micrograms/L, p < 0.005). This response was similar to those after oral ARG-H or ARG-A plus GHRH. No variation was observed in PRL levels after oral ARG (either ARG-H or ARG-A) and/or GHRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Growth rate and growth hormone response to growth hormone-releasing hormone challenge in slowly growing children during chronic administration of clonidine.

In this study the effects of chronic administration of clonidine, an alpha-2-adrenergic agonist, on the growth rate and GH response to GHRH in 12 "slowly growing" children were reported. Clonidine was administered at the dose of 0.04 mg/m2 body surface twice daily along 12 months. The protocol of the study consisted in five periods of growth rate, insulin-like growth factor-1, basal and GHRH-stimulated GH level evaluation: 1) 6-month pretreatment (P1); 2) 6-month placebo administration (PO); 3) after 4 months of therapy (P1); 4) after 4 months of clonidine withdrawal (P2); 5) after 4 months of therapy reinstatement (P3). No difference was observed between P-1 and P0 when all the parameters were considered. During P1 a significant increase of linear growth (p < 0.05 vs P0 and P-1) was observed while standard deviation of height was not modified. At the end of P2, the growth rate and standard deviation of height were similar to those recorded in P0 and P-1. After reinstatement of clonidine therapy a new but less pronounced rise of the growth rate was found (p < 0.05 vs P1, p < 0.01 vs P0 and P-1). GH, insulin-like growth factor-1, GHRH-stimulated GH levels had significantly increased during P1 than P0 and P-1 (p < 0.05), while during P2 they were similar to P0 and P-1. During P3 a new increase of insulin-like growth factor-I baseline and GHRH-stimulated GH levels were observed. However, these were significantly lower than those observed during P1.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Determination by Skeleton↗
PubMed1995

Effects of acute administration of growth hormone-releasing hormone (GHRH) and oxytocin on somatotroph cells in sheep: morphometric study and growth hormone (GH) secretion.

In this work, the combined use of the morphometric study of somatotroph cells and plasma GH levels provided new data for the interpretation of the role played by OT and GHRH on GH cells. GHRH 1-29 (15 micrograms/kg), oxytocin (2.5 IU animal) or 1 ml saline solution were administered to male lambs. The GH plasma concentration was measured by RIA and for the morphometric study the cellular area, nuclear area and volume density of the somatotroph cells were measured in 1 micron semi-thin sections immunolabeled with avidin-biotin technique (ABC). The area under the GH response curve for 3 hours after injection was similar in both saline and OT-treated animals (24.8 +/- 9.1 and 31.4 +/- 14.7 micrograms/ml, respectively) and much lower than that observed in GHRH-treated animals (445.5 +/- 126.7 micrograms/ml). The cell area of somatotrophs was smaller in the GHRH-treated lambs and larger in the OT-treated lambs than in the control lambs (71.47 +/- 1.56, 91.42 +/- 1.72 and 83.1 +/- 1.74 microns 2, respectively). A similar change was observed in the nuclear area; it decreased in the GHRH-treated lambs (21.61 +/- 0.52 microns 2) and increased in the OT-treated lambs (25.45 +/- 0.68 microns 2) with respect to the control group (23.75 +/- 0.44 microns 2). No significant differences were found in volume density.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗