Blunted Growth Hormone Response Research Articles

Mental well-being in alcohol withdrawal: relationship to alpha2-adrenoceptor function.

The possible relationship between postsynaptic alpha2-adrenoceptor function, as assessed by the growth hormone (GH) response to clonidine (CLON) and aspects of mental well-being by self-report of mood using the Swedish Mood Adjective Check List, was investigated in alcohol-dependent patients in the early withdrawal period. Patients had blunted GH responses to CLON and worse mental well-being than control subjects immediately after the end of alcohol intake. No relation was found between mental well-being and postsynaptic alpha2-adrenoceptor function. After 1 week, the GH responses to CLON remained blunted, whereas the state of mental well-being had improved to levels similar to those of control subjects. The results further support a downregulated alpha2-adrenoceptor function during 1 week of alcohol withdrawal. Furthermore, even if subsensitive postsynaptic alpha2-adrenoceptor function was not generally related to state of mood, patients with the lowest postsynaptic alpha2-adrenoceptor function reported the highest levels in the dimensions pleasantness/unpleasantness and activation/deactivation when sober.

Psychopathology in alcohol withdrawal: relationship to alpha2-adrenoceptor function.

The possible relationship between postsynaptic alpha2-adrenoceptor function, as assessed by growth hormone (GH) response to clonidine (CLON; 1.5 or 2.0 microg/kg i.v.), and psychopathology was investigated in 30 patients with alcohol-dependence in the early withdrawal period. Excluding patients with high baseline GH, 23 of the 26 patients had blunted GH responses to CLON and 57% moderate or severe depression at day 1 after the end of alcohol intake. After 1 week, the GH responses to CLON remained blunted in 20 of 21 retested patients, whereas the depression and anxiety remitted in all but two patients. The results do not support any relationship between postsynaptic alpha2-adrenoceptor function and symptoms of psychopathology in alcohol withdrawal.

Blunted Growth Hormone Response to Maximal Exercise in Middle-Aged Versus Young Subjects and No Effect of Endurance Training

The purpose of this study was to evaluate the GH response to exercise and the effects of endurance training on this response in early middle-aged men. Seven healthy middle-aged [M; 42.0 ± 2.4 (±sd) yr old] and five young (Y; 21.2 ± 1.1 yr old) competition cyclists were investigated before and after 4 months of intensive endurance training. Subjects performed an exhaustive incremental exercise test (50 watts for 3 min) with gas exchange measurement, and blood samples for lactate, glucose, and GH determinations were drawn before exercise, at the end of the exercise, and in the recovery phase (1, 3, 5, 10, 15, 20, and 30 min). Basal insulin-like growth factor I was also determined. At exhaustion no differences were found in relative maximal heart rate or blood lactate and glucose peaks. On the contrary, the two groups had markedly different GH responses; in fact, the peak GH response to exhaustive exercise was much lower in M than in Y (8.1 ± 1.3 vs. 57.1 ± 15.5 μg/L; P < 0.01). The training, similar in subjects of the same group, increased progressively from 182 to 300 km/week (+64.8%) in M and from 350 to 600 km/week (+71.4%) in Y. After the training, the percent increase in maximal oxygen consumption was similar in the two groups (M, +15.2%; Y, +17.5%), confirming that the efficiency of the training performed was comparable. In neither group did training have any effect on the GH peak response to exercise, confirming the blunted GH response in M compared to Y (6.7 ± 1.0 vs. 61.0 ± 12.9 μg/L; P < 0.01). Similarly, insulin-like growth factor I concentrations were not significantly affected by training. In conclusion, active middle-aged subjects, compared with the young, showed a blunted GH response to a physiological stimulus such as exercise, indicating that the age-related decline in GH secretion appears in early middle age. This response was not modified by training in either early middle-aged or young subjects.

Association of depressiveness with blunted growth hormone response to maximal physical exercise in young healthy men

Blunted response of growth hormone secretion to several pharmacological challenges is present in depression, but much less is known about the relationship of depression and secretion of growth hormone elicited by physiological stimuli. Furthermore, it is not known whether blunted growth hormone response occurs in depressiveness as measured with psychometric scales. A total of 82 healthy male volunteers (age 18-26 years) exercised on a bicycle ergometer with incremental load to achieve their maximal performance. Before exercise, subjects filled in approbated versions of Beck Depression Inventory (BDI), Spielberger's State-Trait Anxiety Scale, Cohens Perceived Stress Scale, and Schwartzers Self-Efficacy Scale. Blood samples were collected before and after exercise, and growth hormone, cortisol, and testosterone were measured by chemiluminescence immunoassay. Median perceived stress score of the subjects was identical to our population-based database median value, but the subjects had higher self-efficacy and lower depressiveness as shown by median values. In the majority of subjects, physical exercise induced remarkable increases in blood levels of the hormones. Cortisol and testosterone levels were not associated with the scores of psychometric scales. However, growth hormone response was virtually absent in high scorers (above median population score, n = 24) in BDI total score and the negative attitude subcomponent. Hence, this study demonstrates that growth hormone response to physiological stimuli is reduced in psychometrically measured depressiveness.

The effect of body composition on hexarelin-induced growth hormone release in normal elderly subjects.

Growth hormone (GH) release is influenced by several factors including age, gender, physical exercise, nutritional status, sex steroids and body composition. The relationship with body composition is complex. Obesity is accompanied by suppression of spontaneous and stimulated GH release. As increasing body fat reduces stimulated GH secretion following a standard provocative test, the potential clinical uses of GH-releasing peptides (GHRPs), therapeutically or diagnostically, may be dependent on the relationship between body fat and GHRP-stimulated GH release. We have therefore assessed the effect of body composition and gender on the GH releasing capacity of hexarelin. A single bolus of subcutaneous hexarelin at a dose of 1.5 micrograms per kg of body weight was administered at time 0. Blood samples were taken at -10, 0, 10, 20, 30, 40, 50, 60, 90, 120, 170 and 180 min. Twenty-one (eight male) healthy elderly subjects with a median (range) age of 68 (60-81) years and BMI of 26 (19-30) kg/m2 were studied. Dual-energy X-ray absorptiometry (DEXA) was used to assess body composition. Peak GH response correlated negatively with fat mass, BMI, percentage body fat, and weight [r = -0.72, P = 0.0001; r = -0.56, P = 0.009; r = -0.63, P = 0.002 and r = -0.48, P = 0.029, respectively,]. AUC GH correlated negatively with fat mass, BMI and percentage fat mass [r = -0.58, P = 0.006; r = -0.51, P = 0.019 and r = -0.66, P = 0.001 respectively]. Using multiple linear regression, fat mass was the most useful predictor for both peak GH response [R2 = 0.61, P < 0.0001] and AUC GH [R2 = 0.38, P = 0.003]. Gender was not a significant variable. Increasing total fat mass results in a blunted GH response following subcutaneous hexarelin. Total fat mass appears to be a useful predictor of peak GH response even in normal individuals as none of the subjects in the present study was morbidly obese. This indicates that there is a continuum of effect of fat mass on hexarelin-stimulated GH release. Any impact of gender on the GH response to hexarelin is almost certainly indirect and mediated via differences in body composition. This observation will have an impact on the potential diagnostic and therapeutic uses of hexarelin and related GH secretagogues.

Impact of long-term naltrexone treatment on growth hormone and insulin secretion in hyperandrogenic and normal obese patients

The growth hormone (GH) response to stimulation tests is impaired in obesity. Moreover, obese patients exhibit a “paradoxical” increase of GH to GH-releasing hormone (GHRH) stimulation after food ingestion; this paradoxical response is reversed by naloxone infusion. On the other hand, β-endorphin seems to exert profound effects on insulin release. Recent studies also demonstrated an impairment of GH response to several stimuli in polycystic ovary syndrome (PCOS), a condition associated with obesity, hyperinsulinism, and insulin resistance. Chronic inhibition of opioid tone by the opioid antagonist naltrexone (NTX) is able to reduce the insulin response to an oral glucose tolerance test (OGTT) in hyperinsulinemic PCOS patients. Since insulin and GH may reciprocally influence their secretion and the opioid system may have a role in the pathogenesis of hyperinsulinemia and reduced GH secretion, we have explored the involvement of these neuroendocrine mechanisms in essential obesity and in obesity associated with hyperandrogenism by a long-term treatment with an opiate antagonist. We tested seven obese patients affected by PCOS, seven matched women with essential obesity (EO), and five non-obese control subjects. All patients, in the follicular phase, underwent an OGTT (75 g) and basal hormone assay. Two days later, patients were subjected to a GHRH test. The patients then had 4 weeks of treatment with NTX 50 mg/d. Following continuation of the treatment, OGTT and GHRH tests were repeated. Insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) plasma concentrations were also determined in the basal condition before and after NTX treatment. NTX treatment reduced fasting insulin levels in patients with EO ( P < .05) and restored a normal GH response to GHRH without affecting IGF-1 and IGFBP-3 levels. In PCOS subjects, NTX reduced the insulin response to a glucose load and failed to modify the blunted GH response to GHRH. Our data suggest a significant difference in opioid system function in PCOS and EO subjects, indicating a particular form of obesity in PCOS. The opiate antagonist treatment in EO may act through the reduction of negative insulin feedback on GH secretion. In PCOS patients, the failure to improve GH secretion in obese hyperandrogenized patients may be related to a high opioidergic tone or to the inhibitory predominance of other neurotransmitters.

Stressful life events influence nocturnal growth hormone secretion in depressed children

Pharmacologic challenge studies of growth hormone (GH) secretion in depressed children, adolescents, and adults have consistently reported blunted GH responses (Ansseau et al 1984; Jarrett et al 1990; Puig-Antich et al 1984a; Ryan et al 1988, 1994). In contrast, studies of baseline nocturnal (or sleep stimulated) GH have revealed varied results across age groups. Studies of depressed adults have found blunted nocturnal GH secretion in recurrent depressives (Jarrett et al 1990; Steiger et al 1989; Voderholzer et al 1993), which remains blunted over time (Jarrett et al 1994) and predicts recurrence (Franz et al 1995); however, the findings from nocturnal GH studies in depressed children and adolescents have been inconsistent. In an early report, Puig-Antich et al (1984b) found that depressed children hypersecreted GH during sleep compared to controls. In contrast, a larger study of prepubertal depressed children found no differences in nocturnal GH secretion compared to normal controls (DeBellis et al 1995). One study of depressed adolescents found nocturnal GH to be elevated (Kutcher et al 1988). Another study of adolescents found no differences in GH secretion between depressed and normal controls during the night (Dahl et al 1992), but a subgroup of suicidal depressed adolescents did show blunted nocturnal GH (Dahl et al 1992). Since age has been shown to effect GH secretion beginning in early adolescence (Copinschi and Van Canter 1995), it is possible that maturational changes in GH regulation associated

Psychopathological and behavioral correlates of dopaminergic sensitivity in alcohol-dependent patients.

To explore 2 facets of dopamine receptor sensitivity in alcoholics: (1) whether reduced sensitivity of central dopamine receptors is correlated with anxiety, depression, or novelty seeking and (2) whether this reduction is associated with poor treatment outcome. Sixty-four alcohol-dependent patients were assessed according to their clinical outcome, sensitivity of central dopamine receptors (apomorphine-induced growth hormone secretion), mood states, and personality traits before and after detoxification. Patients with poor treatment outcome displayed a blunted growth hormone response before, but not after, detoxification. Growth hormone response was not significantly correlated with novelty seeking. Relapsing patients tended to be less depressed than patients who remained abstinent during observation. This study did not support the hypothesis that reduced sensitivity of dopamine receptors is associated with anxiety, depressed mood, or high novelty seeking in alcoholism.

Noradrenergic mechanisms in stress and anxiety: II. Clinical studies

Studies in animals have shown a relationship between alterations in noradrenergic brain system function and behaviors of anxiety and fear. These findings have generated the hypothesis that the symptoms seen in patients with anxiety disorders may be related to alterations in noradrenergic function. A number of clinical studies have tested this hypothesis, utilizing measures of catecholaminergic function such as heart rate and blood pressure, measurement of norepinephrine and its metabolites in urine and plasma and adrenergic receptor binding in platelets, as well as pharmacological challenge to the noradrenergic system. Acute stressors, such as public speaking, have been associated with an increase in heart rate, blood pressure, and norepinephrine and its metabolites in urine and plasma. Findings in patients with panic disorder at baseline related to heart rate, blood pressure, baseline norepinephrine and its metabolites, and platelet adrenergic receptors have been mixed, while the most consistent findings have been blunted growth hormone response to clonidine and increased 3-methoxy-4-hydroxy-phenylethylene-glucol (MHPG) and anxiety following stimulation of the noradrenergic system with yohimbine. Baseline measures of noradrenergic function in patients with posttraumatic stress disorder (PTSD) have also been mixed, while an increased heart, blood pressure and norepinephrine response to traumatic reminders, as well as increased behavioral (as well as different brain metabolic) response to yohimbine, have been found in PTSD. There are fewer studies of noradrenergic function in the other anxiety disorders, and the findings there have not been consistent. These studies provide evidence for increased noradrenergic responsiveness in panic disorder and PTSD, although there does not appear to be an alteration in baseline noradrenergic function in these patients. © 1996 Wiley-Liss, Inc.

Noradrenergic mechanisms in stress and anxiety: II. Clinical studies

Studies in animals have shown a relationship between alterations in noradrenergic brain system function and behaviors of anxiety and fear. These findings have generated the hypothesis that the symptoms seen in patients with anxiety disorders may be related to alterations in noradrenergic function. A number of clinical studies have tested this hypothesis, utilizing measures of catecholaminergic function such as heart rate and blood pressure, measurement of norepinephrine and its metabolites in urine and plasma and adrenergic receptor binding in platelets, as well as pharmacological challenge to the noradrenergic system. Acute stressors, such as public speaking, have been associated with an increase in heart rate, blood pressure, and norepinephrine and its metabolites in urine and plasma. Findings in patients with panic disorder at baseline related to heart rate, blood pressure, baseline norepinephrine and its metabolites, and platelet adrenergic receptors have been mixed, while the most consistent findings have been blunted growth hormone response to clonidine and increased 3-methoxy-4-hydroxy-phenylethylene-glucol (MHPG) and anxiety following stimulation of the noradrenergic system with yohimbine. Baseline measures of noradrenergic function in patients with posttraumatic stress disorder (PTSD) have also been mixed, while an increased heart, blood pressure and norepinephrine response to traumatic reminders, as well as increased behavioral (as well as different brain metabolic) response to yohimbine, have been found in PTSD. There are fewer studies of noradrenergic function in the other anxiety disorders, and the findings there have not been consistent. These studies provide evidence for increased noradrenergic responsiveness in panic disorder and PTSD, although there does not appear to be an alteration in baseline noradrenergic function in these patients.

Studies of serotonin function in anorexia nervosa

Neuroendocrine, temperature, test-meal, and psychometric responses are reviewed following challenges with the post-synaptic 5-HT receptor agonist m-chlorophenylpiperazine ( m-CPP), the 5-HT precursor l-tryptophan ( l-TRP), and placebo in 12 patients with anorexia nervosa (AN) and 16 healthy controls. A subset of the AN patients ( n = 8) were rechallenged 3–4 weeks after attaining a predetermined goal weight. AN patients had blunted prolactin (PRL) responses to both m-CPP and l-TRP at low-weight and at goal-weight in comparison to controls, although there was a tendency toward normalization with weight gain. There were trends for blunted growth hormone (GH) responses following both l-TRP and m-CPP in the low-weight but not the goal-weight AN patients. Cortisol (CORT) responses following m-CPP and l-TRP were not significantly different among any of the groups. Temperature and test-meal measures were largely unaffected by serotonergic agents in the patients, although m-CPP decreased meal size in the controls. Psychometric responses were variable and are briefly described. Taken together, these findings indicate that responsiveness in post-synaptic hypothalamic-pituitary serotonergic pathways is altered in AN patients. Although there were some trends toward normalization of responsiveness following goal-weight attainment, many differences tended to persist in the patients despite an average increase of 13 kilograms. These may represent changes in serotonergic function at levels in the CNS “above” the hypothalamus.

Evidence for reduced dopamine D2 receptor sensitivity in postwithdrawal alcoholics.

Dopamine D2 receptor sensitivity was assessed in the postwithdrawal period in alcoholics. Growth hormone (GH) responses to dopamine D2 agonist bromocriptine were measured in eight DSM-III-R alcohol-dependent subjects who were 2 weeks or more postalcohol withdrawal. Their responses were compared with eight nonalcoholic controls. After an overnight fast, each subject received 1.25 mg of bromocriptine orally, and serial samples of GH were taken over a 3-hr period. There was a significantly blunted delta GH response (mean +/- SE) in the alcoholic group, 2.3 mU/liter (+/- 1.4) relative to controls, 7.7 mU/liter (+/- 1.2) (t = 2.96, df = 14, p = 0.01). There was a significantly blunted peak GH response (mean +/- SE) in the alcoholic group, 5.36 mU/liter (+/- 2.1) relative to controls, 9.04 mU/liter (+/- 5.0). This difference also reached statistical significance (t = 2.32, df = 14, p = 0.035). A repeated-measures ANOVA yielded a significant within-subjects effect of time [F(4,54) = 4.08, p = 0.0057], a significant within-subjects effect of group [F(1,14) = 5.6, p = 0.0329], and an almost significant group x time interaction [F(4,54) = 2.45, p = 0.056]. This result implies a relative dopamine D2 receptor subsensitivity in alcoholics in the postwithdrawal period.

Alcohol dependence, family history, and D2 dopamine receptor function as neuroendocrinologically assessed with apomorphine

Fifteen alcohol dependent men with an alcohol dependent first degree relative (i.e. family history positive or FHP), 15 well matched alcohol dependent men without a family history for alcohol dependence (i.e. family history negative or FHN), and 15 healthy controls (CONTR) participated in this study. The three groups were compared according to their postsynaptic D2 dopamine receptor function as assessed by growth hormone release after stimulation with the dopamine receptor agonist apomorphine. Statistical evaluation was done by planned comparisons within a one-way ANOVA. Alcohol dependent subjects significantly differed from CONTRs as long as family history was not taken into account ( t(42) = 2.38; P = 0.022∗). When differentiating according to family history, both FHPs and FHNs maintained a blunted growth hormone response. However, the difference between FHNs and CONTRs, though present, dropped out of statistical significance ( t(42) = 1.65; P = 0.105); at the same time, the difference between FHPs and CONTRs became slightly stronger ( t(42) = 2.47; P = 0.017∗). In conclusion, our data give neuroendocrinological support to the assumption that a reduced D2 dopamine receptor function in alcohol dependent men is not only a state marker of residual heavy drinking but also a genetically determined trait marker.

In vivo evidence of a positive role for somatostatin to optimize pulsatile growth hormone secretion.

Despite convincing evidence that somatostatin (SRIF) and growth hormone (GH)-releasing factor (GRF) individually play crucial roles in GH regulation, the nature of the interplay between these two hypothalamic hormones is far from clear. In the present study, we used the long-acting SRIF analogue, octreotide, as a probe in both the normal and mutant dwarf (dw) rat 1) to further elucidate the temporal nature of the SRIF-GRF interaction in vivo and 2) to define possible mechanisms of action of SRIF in generating pulsatile GH secretion. Normal free-moving adult male rats pretreated with octreotide (25 and 50 micrograms iv) and subsequently challenged with GRF (1 micrograms iv) exhibited a markedly blunted GH response to exogenous GRF 1 h after treatment. In contrast, preexposure to octreotide for 3 h produced a two- to threefold augmentation in GH responsiveness to GRF. Compared with normal saline-pretreated controls, 3-h pretreatment with octreotide produced a 14- to 16-fold augmentation in the postinhibitory rebound release of GH after the coadministration of native SRIF-14 and GRF (P < 0.001). In dw rats, which show a selective reduction in GH synthesis and storage, 3-h preexposure to octreotide failed to significantly alter GRF-induced GH release. These results demonstrate that, in the normal male rat, a 3-h period of exposure to the SRIF analogue octreotide is sufficient to enhance GH responsiveness to GRF. Our findings suggest that this effect is due to a SRIF-mediated buildup of pituitary GH stores in a readily releasable poo.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth hormone response to growth hormone-releasing hormone and clonidine in depression

Growth hormone (GH) responses to the alpha 2-adrenoceptor agonist clonidine and to GH-releasing hormone (GHRH) were measured in 12 patients fulfilling DSM-III-R criteria for major depressive disorder and in 12 age- and sex-matched controls. GH responses to clonidine correlated significantly with the GH responses to GHRH in the depressed patients as well as in the controls. Neither the responses to clonidine nor the responses to GHRH were significantly lower in depressed patients than in controls. Similarly, somatomedin-C (Sm-C) plasma concentrations and baseline GH concentrations were not different between the two groups. The data do not suggest that blunted GH responses to clonidine and/or GHRH represent specific features of depression.

Growth-Hormone Response to Clonidine in Panic Disorder Patients in Comparison to Patients with Major Depression and Healthy Controls

Growth-hormone (GH) responses to the alpha 2-adrenoceptor agonist clonidine were measured in 9 panic disorder patients, in 9 patients fulfilling DSM-III-R criteria for major depressive episode, and in 9 age- and sex-matched controls. GH responses to clonidine were not significantly different between the groups. The data do not agree with the assumption that blunted GH responses to clonidine represent a general feature of panic disorder or major depression.

Hypothalamic Mediation of Reduced GH Secretion in Diabetic Rats: Evidence for Reduced Cholinergic Inhibition of Somatostatin Release

The Goto-Kakizaki (GK) rat is a new model of diabetes mellitus and in this study we have characterized the diabetic and growth hormone (GH) secretory status of male GK rats at 6 and 16 weeks of age. We have also investigated the role of endogenous somatostatin (SS) and cholinergic manipulation on the GH responses to GH-releasing hormone (GHRH). GK rats were non-obese with significant fasting hyperglycaemia, hyperinsulinaemia and absent insulin responses to IV glucose. The GH response to GHRH was reduced at 16 weeks compared with normal, age-matched Wistar rats but no differences were observed at 6 weeks. Pretreatment of older rats (16 weeks) with anti-somatostatin antibodies (SS-Ab) significantly increased GH responses to GHRH in both normal and GK groups. Cholinergic augmentation with pyridostigmine (PD) reversed the blunted GH responses to GHRH in older GK rats but had no effect in the normal or young (6 weeks) GK rats. These results indicate that SS release mediates the blunted GH response to GHRH in GK rats and that reduced hypothalamic cholinergic signalling to the somatostatinergic neurone may mediate the increase in SS release. This view is supported by the results from in vitro studies in which cholinergic muscarinic blockade with pirenzepine (PIR) caused dose-related stimulation of SS release from normal rat hypothalami but was without effect on GK rat hypothalami. The cause of this alteration in hypothalamic function is, at present, unknown.

Blunted GH Response to Growth Hormone-Releasing Hormone (GHRH) Alone or Combined with Arginine in Non-Insulin-Dependent Diabetes Mellitus

An increased spontaneous and stimulated growth hormone (GH) secretion is well documented in insulin-dependent diabetes mellitus. On the contrary, in non-insulin-dependent diabetes mellitus (NIDDM) conflicting results arise from literature. In 14 patients with NIDDM, 7 normal weight (NWD) and 7 obese (OD), we investigated the somatotrope responsiveness to GHRH (1 microgram/kg) alone or combined with arginine (ARG, 0.5 g/kg), which is able to enhance the GH response to GHRH, probably by inhibiting somatostatin release from hypothalamus. Baseline IGF-I, IRI FFA and glucose levels were also determined. Twelve healthy normal subjects (NS) and 12 obese patients (OP) were evaluated as control groups. GH but not IGF-I levels were higher (p < 0.05) in NS than in OP (1.5 +/- 0.5 vs 0.5 +/- 0.2 microgram/l). Insulin levels were higher (p < 0.05) in OP than in NS, NWD and OD (18.7 +/- 1.8 vs 8.7 +/- 0.5, 6.4 +/- 1.9 and 11.8 +/- 1.2 microU/l). FFA were higher (p < 0.05) in NWD. OD and OP than in NS (0.69 +/- 0.04, 0.70 +/- 0.04 and 0.65 +/- 0.06 vs 0.39 +/- 0.03 mmol/l). Plasma glucose was higher (p < 0.05) in diabetic patients than in normal and obese subjects. GH responses to GHRH in NWD, OD and OP were similar (AUC: 221.6 +/- 33.3, 206.0 +/- 35.9 and 177.2 +/- 57.3 micrograms/l/min, respectively) and all lower (p < 0.05) than that in NS (776.7 +/- 206.5 micrograms/l/min). ARG determined a significant increase of GHRH-induced GH release in all groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Noradrenergic and dopaminergic interrelation in schizophrenia

Growth hormone (GH) and prolactin (PRL) responses to the acute administration of clonidine (150 μg) and apomorphine (0.5 mg) were investigated in parallel in 20 drug-free subchronic and chronic sghizophrenic patients and in nine control subjects. Neither basal levels of the two hormones nor their mean responses to both stimuli differed significantly between the two groups. However, eight patients had blunted GH responses to clonidine and seven to apomorphine; only two patients showed blunted GH responses to both stimuli. The blunted GH response to apomorphine correlated with the chronicity of the disorder. A greater than normal GH response to clonidine stimulation was observed in paranoid patients. Significant correlations were observed between negative symptoms and GH responses to clonidine (negative), between negative symptoms and PRL responses to apomorphine (positive), and between positive symptoms and PRL responses to apomorphine (negative).

Chronic baclofen therapy improves the blunted growth hormone response to intravenous arginine in subjects with spinal cord injury

Chronic baclofen therapy improves the blunted growth hormone response to intravenous arginine in subjects with spinal cord injury