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J Devesa

Publications and source records attributed to J Devesa.

At least 37 records · Page 2Linked to original sources
PubMed1991

Evidence that alpha 2-adrenergic pathways play a major role in growth hormone (GH) neuroregulation: alpha 2-adrenergic agonism counteracts the inhibitory effect of muscarinic cholinergic receptor blockade on the GH response to GH-releasing hormone, while alpha 2-adrenergic blockade diminishes the potentiating effect of increased cholinergic tone on such stimulation in normal men.

The aim of this study was to investigate the interrelationships between alpha 2-adrenergic and cholinergic pathways in the control of hypothalamic somatostatin (SRIF) secretion in humans. In eight normal volunteers subjects we compared the pattern of GHRH-induced GH release to that elicited by similar challenge given 60 min after a pretreatment with drugs affecting alpha 2-adrenergic and muscarinic cholinergic neurotransmission. In a control study, synthetic GHRH [GRF-(1-29); 1 microgram/kg, iv] was administered 60 min after giving placebo. In other experiments, the administration of atropine (1 mg, im), or clonidine (0.300 mg, orally), or atropine plus clonidine, or pyridostigmine (120 mg, orally), or yohimbine (30 mg, orally), or pyridostigmine plus yohimbine, at 0 min was followed by GHRH administration 60 min later. The administration of both clonidine and pyridostigmine significantly (P less than 0.01) enhanced the GH responses to GHRH compared to those elicited by this challenge when given after placebo. Conversely, atropine pretreatment significantly (P less than 0.01) blocked the GH response to GHRH challenge, whereas yohimbine did not significantly affect it. When atropine and clonidine were given together, the inhibitory effect of the former was overcame and mean GHRH-elicited GH peak response was significantly (P less than 0.05) higher than that in the control study. In contrast, pretreatment with yohimbine significantly (P less than 0.05) blunted the pyridostigmine-induced enhancement of GHRH-elicited GH release. These data confirm our previous postulate suggesting that the stimulatory effect of clonidine on GH release is mainly exerted by inhibiting the hypothalamic SRIF release. Moreover, the effect of cholinergic neurons on SRIF release seems to be, at least in part, dependent on alpha 2-adrenergic pathways. Based on these data, it can be proposed that the alpha 2-adrenergic system plays a major role in the control of hypothalamic SRIF release, and hence in GH neuroregulation, whereas the muscarinic cholinergic system would participate in such regulation by modulating the functional activity of the former.

Adult↗
PubMed1990

Synergistic effect of growth hormone-releasing hormone (GHRH) and clonidine in stimulating GH release in young and old dogs.

The effect of acute administration of growth hormone-releasing hormone (GHRH), clonidine (CLO), an alleged GHRH releaser, or GHRH and clonidine given simultaneously was studied in young and old dogs. Simultaneous administration of CLO induced in young dogs an additive effect on GH release and potentiated in old dogs the GHRH-induced GH release, with the GH response being clearly higher than the sum of the GH responses to GHRH or CLO alone. These data suggest that CLO promotes GH release in the dog also by inhibition of somatostatin release.

Aging↗
PubMed1990

Study of the source(s) of hyperandrogenism in women with idiopathic hirsutism.

22 women with Idiopathic Hirsutism (IH) were studied in terms of their basal levels of total (tT) and free (fT) testosterone, dehydroepiandrosterone sulphate (DHEA-S) estradiol, androstenedione (Adione), LH and FSH. The gonadotropin response to GnRH was also studied. These studies were repeated after treatment for 30 days with buserelin, i. n., 900 micrograms/dya. It was observed that the reduction in fT after buserelin varied from nil to 79% of decrease over the baseline values. The suppression of fT (and also of tT and Adione) was normally distributed. Therefore, there was no evidence to suggest the presence of a non-suppressible "adrenal group" and of a suppressible "ovarian group". Interesting, and hitherto unreported, findings were the significant correlations between the percentual reduction of fT and tT and the pre-buserelin LH responses to GnRH. It is therefore suggested that both LH response to GnRH and androgen suppression after buserelin are markers of the degree of ovarian contribution to the androgen pool. Neither of these parameters correlated with basal tT, fT, Adione or body mass index, casting some doubts on the theorization that the LH hyperresponsiveness observed in IH or PCO are secondary to conditions that predispose to increased exposure to androgen-derived estrogens.

Adolescent↗
PubMed1990

Alpha 2-adrenergic agonism enhances the growth hormone (GH) response to GH-releasing hormone through an inhibition of hypothalamic somatostatin release in normal men.

The purpose of this study was to investigate the precise mechanism by which central alpha 2-adrenergic pathways modulate GH secretion in humans. In 10 normal subjects we compared the pattern of clonidine-induced GH release to that elicited by GH-releasing hormone (GHRH) given at a time of presumably similar responsiveness of the somatotrope. We also evaluated the effect of stimulation by GHRH (either endogenous, by administration of clonidine, or exogenous) on the GH response to a further exogenous GHRH stimulation. In 2 experiments the administration of clonidine (0.150 mg, orally) at 0 or 60 min was followed by a GHRH [GRF-(1-29); 1 micrograms/kg, iv] challenge at 180 min. In other experiments subjects received on separate occasions placebo or clonidine at 0 min, followed by GHRH at 60 min and again at 180 min. In a further experiment the administration of clonidine at 0 min was followed by 2 GHRH challenges (60 and 180 min later). The administration of clonidine 60 or 120 min, but not 180 min, before the GHRH bolus significantly (P less than 0.01) increased the GH responses to this challenge compared to those elicited by GHRH when given after placebo in a period of a similar somatotrope responsiveness. These, in turn, were significantly (P less than 0.05) higher than those elicited by clonidine alone. The close relationship between pre-GHRH plasma GH values and GHRH-elicited GH peaks, not observed for clonidine, was lost after pretreatment with this drug. These data indicate that clonidine was able to disrupt the intrinsic hypothalamic-somatotroph rhythm, suggesting that alpha 2-adrenergic pathways have a major inhibitory effect on somatostatin release. Our data also indicate that GH responses to a GHRH bolus administered 120 min after a prior GHRH challenge are dependent on two parameters: the intrinsic hypothalamic-somatotroph rhythm at the time of the second GHRH bolus, and the magnitude of GH secretion elicited by the previous somatotroph stimulation. In summary, alpha 2-adrenergic agonism appears to act primarily in GH control by inhibiting the hypothalamic release of somatostatin, rather than by stimulating GHRH secretion.

Adolescent↗
PubMed1989

Effects of bromocriptine on pituitary and adrenal cortex in pre-adrenarchal rabbits.

The effect of bromocriptine on the morphological picture and steroid content of the adrenal gland, and on certain pro-opiomelanocortin (C) peptides in the pituitary gland was evaluated in preadrenarchal rabbits. Eighteen immature male rabbits (5 weeks of age), were treated for 10 days with saline (n = 10,2 ml sc) or bromocriptine mesylate (n = 8, 3 mg/kg sc) two times/day. After the last administration all animals received dexamethasone (0.25 mg im) and the next morning, 60 min after ACTH injection (0.25 mg im), plasma was drawn and they were sacrificed. Adrenals and pituitaries were immediately removed. For each animal, one adrenal gland was fixed, dehydrated and embedded in paraffin for histology; the other one was stored in saline for determination of androstenedione (A), dehydroepiandrosterone (DHA), 17-OH progesterone (17 P), and cortisol. Steroids were analyzed by RIA after previous extraction and celite-ethyleneglycol chromatography, or directly (cortisol). The immunoreactivities (ir) related to beta-Endorphin (B-EP), ACTH and alpha-MSH were evaluated in pituitary homogenates using specific RIAs. The bromocriptine-treated rabbits showed a significant increase in the percentage of the adrenal zona reticularis (21.5 +/- 3.9% of total cortex vs. 12.7 +/- 1.3% in controls, p less than 0.05, mean +/- SE), and a decrease of the zona fasciculata (57.6 +/- 3.13% vs. 67.7 +/- 2.05% in controls, p less than 0.05). No significant changes were observed in the relative percentage of the zona glomerulosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1989

Reasons for the variability in growth hormone (GH) responses to GHRH challenge: the endogenous hypothalamic-somatotroph rhythm (HSR).

The aims of this study were: (1) to test the possibility that pre-GHRH plasma GH values could reflect the functional status of the hypothalamic-somatotroph rhythm (HSR) at testing, and thus explain if it is responsible for the marked variability in GH responsiveness to GHRH challenge and (2) to see if exogenous somatostatin (SS) could disrupt this endogenous HSR and thus make the GH responses homogeneous. (1) Two to 14 GHRH acute tests (GRF-29, 1 micrograms/kg, i.v. bolus) were performed in 12 normal men and 10 normal women at the same time (0830 h) at random intervals (2 to 60 days). Blood samples to measure plasma GH were drawn at 15 min intervals before and after GHRH challenge. Given that the increments in pre-GHRH plasma GH values (I = value at 0 min minus value at -15 min) were highly correlated with either GHRH-elicited peaks of GH (men, r = 0.81; women; r = 0.69; P less than 0.0001) or the rise in GH after the challenge (r = 0.685; P less than 0.0001, in the total of tests performed), three theoretical HSR phases were proposed: (A) I greater than or equal to 0.4 microgram/l Secretory Phase; (B) I less than or equal to 0, (from GH at -15 min greater than or equal to 1.5 microgram/l), Secretion Plateau; (C) I less than or equal to 0, (from GH at -15 min less than or equal to 1.5 microgram/l), Refractory Phase. Individually, 91% of the men and 86% of the women showed a constant HSR phase when tested at the same time of day independently of the intervals between tests. GH responses (peaks, mean +/- SEM, g/l) in Phase A (women, 51.5 +/- 4.1; men, 31.4 +/- 3.2) were significantly higher (P less than 0.01) than those in Phase B (women, 22.6 +/- 1.8; men, 19.7 +/- 1.5), and these than those in Phase C (women, 9.2 +/- 1.5; men, 6.2 +/- 0.5). The great dispersion observed when GH peaks were analysed as a whole disappeared (except in Phase A in women) when they were evaluated according to the HSR Phase at testing. (2) In seven men and eight women 7 min after stopping an infusion of SS (250 micrograms/h for 3 h) a new GHRH test was performed. Plasma GH variations prior to SS infusion expressed the previous HSR Phase, while the GHRH-elicited peak of GH established the Phase at the moment of testing.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

Growth hormone (GH) responsiveness to GHRH in normal adults is not affected by short-term gonadal blockade.

The effects of changes in circulating gonadal steroids on GH secretion elicited by GHRH challenge (1 microgram/kg) in normal adults volunteers (aged 18-24 years), were evaluated in 10 women and 10 men before and after gonadal blockade was achieved by a GnRH agonist (1500 micrograms/day by nasal spray for 40 days). To see if the effect of testosterone on GH secretion was dependent on its aromatization to estradiol (E2), GHRH tests were performed in 7 normal men prior to administration of testosterone enanthate (250 mg im), 8 days after this treatment had began, and again after E2 receptor blockade with tamoxifen (30 mg for 2 days plus 10 mg on the third day 2 h before the GHRH test, po) administered 8 days after testosterone enanthate. The study of the functional status of the somatotropes at the time of GHRH testing was made according to our previous postulate. Short-term gonadal blockade did not affect the parameters of GH response to GHRH in neither women nor men. Thus, the functional blockade of the gonads may be advisable as an adjunct therapy in the treatment of hypothalamic GH-deficiency during the peripubertal stage. In the other group of men, administration of testosterone enanthate significantly increased GHRH-elicited GH release, but this was reverted after E2 receptor blockade. Since the hypothalamic-somatotrope rhythm was altered by both these pharmacological manipulations, it appears that testosterone acts on GH release mainly at the suprapituitary level, and that this action is secondary to its aromatization to E2.

Adolescent↗
PubMed1988

Inhibitory effect of cabergoline on the development of estrogen-induced prolactin-secreting adenomas of the pituitary.

Cabergoline 1-[(6-allylergolin-8 beta-yl)carbonyl]-1-[3-(dimethylamino) propyl]-3-ethylurea is a recently developed ergot derivative with a long-lasting dopamine agonist action. We now studied the ability of cabergoline to counteract the development of a prolactin-secreting tumor (prolactinoma) induced in female rats by long-term administration of high doses of estrogens. The effect of cabergoline was compared to that of bromocriptine. Cabergoline (0.6 mg/kg p.o.) had a marked and sustained prolactin-lowering effect in freely moving female rats, its effect still being present 3 days after a single dose. Bromocriptine, at a dose 5-fold higher (3 mg/kg s.c.), induced a strong and short-lasting prolactin inhibitory effect which, however, had completely disappeared 24 h post-injection. Intermittent administration of cabergoline (0.6 mg/kg p.o. every 3 days), starting from the first day of estrogen treatment, completely counteracted the development of the prolactinoma, as judged by the weight of the pituitary and the stimulating effect of estrogens on plasma prolactin and mitotic rate and DNA synthesis of pituitary cells. These effects of cabergoline were shared by a 5-fold higher dose of bromocriptine (3 mg/kg s.c.) given daily. The potent anti-tumorigenic effect of cabergoline, coupled to a sustained prolactin-lowering effect, the most prolonged ever seen with an ergot derivative, makes cabergoline a most suitable drug for the treatment of human macroprolactinomas.

Adenoma↗
PubMed1988

Adrenal androgen secretion and dopaminergic activity in anorexia nervosa.

The aim of the present study was to investigate if the postulated deficient adrenal androgen secretion in Anorexia Nervosa (AN), could be associated with a status of sustained dopaminergic hyperactivity. The adrenal responses to ACTH and PRL response to dopaminergic receptor blockade were studied in seven patients with Anorexia Nervosa and seven regularly menstruating women. AN patients showed lower baseline DHEA-sulphate (DHEA-S), androstenedione (Adione) and prolactin (PRL) levels than controls. The response to ACTH revealed evidences of significantly decreased 17-20 desmolase activity in AN, with apparent predominance of glucocorticoid over androgenic pathways relative to controls. Because dopaminergic receptor blockade with Domperidone (DOM) showed intense dopaminergic hyperactivity in AN, we postulate that the adrenal regression seen in the disease is the consequence of a reduced zona reticularis as a consequence of the lack of trophic support by PRL and/or intermediate lobe proopiomelanocortin (IL-POMC). This is consistent with our previous results in pre-adrenarchal dogs and rabbits.

Adolescent↗
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

Dopamine acts on acetylation of proopiomelanocortin-derived products in dog pituitary.

The effect of chronic dopaminergic receptor blockade using domperidone (DOM) on the immature dog pituitary content of POMC-related peptides was evaluated. Six immature dogs were treated with DOM for 15 days, 3 times/day, po (3 mg/kg) together with DOM sc (0.6 mg/kg) at 21.00 h. Placebo was administered to six control animals with the same protocol. On the 16th day, the animals were killed, the whole pituitary removed, homogenized, and submitted to reverse-phase HPLC purification prior to radioimmunoassay (RIA) evaluation of beta-endorphin, ACTH and alpha-MSH immunoreactivities (ir). DOM-treated dogs showed a pituitary concentration of beta-EP and ACTH similar to the placebo-treated dogs. The total alpha-MSH ir was similar in both groups and distributed on two main peaks: one corresponding to alpha-MSH and another coeluting with des-acetyl-alpha-MSH [1-13(ACTH)NH2]. However, the percentage of alpha-MSH on total ir in DOM-treated dogs (15.4 +/- 2.6%) was lower than in controls (37.5 +/- 4.5%, P less than 0.01); the corresponding percentage of 1-13(ACTH)NH2 content was 63.0 +/- 3.8% vs 44.7 +/- 3.7%, (P less than 0.01). The alpha-MSH/1-13(ACTH)NH2 ratio was considerably decreased by the treatment (0.25 +/- 0.06 vs 0.89 + 0.15, P less than 0.01). Acetyl beta-EP-like ir was also lower in treated (38.4 + 5.4 fmol/mg) vs control (86.6 + 19.2 fmol/mg, P less than 0.05) animals. These data indicate that the dopaminergic system plays an important role in the control of acetylation processes of POMC-related peptides in the pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗
PubMed1987

Steroids and neuroendocrine function in anorexia nervosa.

Anorexia nervosa is a primarily psychiatric syndrome of self-induced weight loss due to an intense fear of becoming obese. Numerous endocrine abnormalities occur in anorexia nervosa patients, and in many respects these alterations reflects the endocrinology of reduced energy intake. However, the basic mechanisms of those alterations are far from being understood. In an attempt to understand the disrupted mechanisms of the hypogonadotropic hypogonadism of the anorectic state, we studied 10 anorectic women in the acute phase of their illness; all met the DSM III criteria. On each patient, two tests were performed with either saline as control or infusion of the opioid antagonist naloxone, and both LH and FSH levels were measured. Four mg of naloxone as bolus was used, followed by a naloxone infusion of 2 mg/h for 4 h. Compared with the pattern of normal women, naloxone did not increase in the anorectic patients either LH or FSH levels nor pulsatility. This result suggests that endogenous opioid peptides are not implicated in the low gonadotropic situation of anorexia nervosa. An alternative explanation could be that the low estrogenic "milieu" of these patients could mask the opioid action. To test this second possibility, another group of 7 anorectic women after partial weight recovery were challenged with estrogen administration. Compared with the pattern of normal women volunteers, all the anorectic patients but one presented an abnormal response in both LH and FSH levels after estrogen administration. In fact, the negative feedback and the delayed positive feedback of LH after estrogen were absent in these patients. Interestingly enough, the only patient with near-normal LH response to estrogen was considered fully recovered by the Psychiatric Unit. Several alterations in the hypothalamic-pituitary-adrenal axis has been reported in anorexia nervosa. Seven anorectic patients and 7 aged-matched women were challenged by ACTH 1-24, 250 micrograms (i.v.) and the ratio of increments in adrenal steroid products to precursors monitored. ACTH-induced increments in cortisol with respect to increments in 17-OH-progesterone was similar in anorectics and controls. On the contrary, the ratio of increments of androstenedione with respect to increments in 17-OH-progesterone were greater in anorexia nervosa than controls. These results suggest that in anorexia nervosa the 11-beta-21-alpha-hydroxylase system is normal but a deficient 17-20 desmolase system is present. Finally, the altered pattern of GH secretion in anorexia was studied using GHRH (1 microgram/kg) as stimulus of pituitary GH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Amenorrhea↗
PubMed1987

Morphological and functional stimulation of adrenal reticularis zone by dopaminergic blockade in dogs.

In order to investigate factors affecting adrenal maturation leading to adrenarche, the effect of dopaminergic blockade on the morphology and function of the adrenal reticularis zone was studied in fourteen preadrenarchal dogs. Seven animals of 7 weeks of age (adrenarche at 11 weeks) were treated with domperidone (DOM) 3 times/day p.o. (3 mg/kg) at 09.00 h, 14.00 h, and 21.00 h, plus an additional injection of DOM s.c. (0.6 mg/kg) at 21.00 h for 15 days. Seven control animals received diluent. Twelve hours after the last injection, dogs received 0.25 mg ACTH i.m. and were sacrificed 60 min later. Blood was collected and adrenals removed. After histological evaluation, the percent of the reticularis, fasciculata, and glomerulosa zones with respect to the total cortex was calculated. Plasma androstenedione (A), dehydroepiandrosterone (DHA), 17-OH-progesterone (17P), and cortisol (F) levels in response to ACTH were also assessed. DOM-treated dogs show a significant development of the zona reticularis compared to control animals (19.2 +/- 0.6% vs 8.8 +/- 2.09% respectively, X +/- SE, P less than 0.01). In the same animals, the DHA response to ACTH (9.0 +/- 1.6 ng/dl) was significantly higher than in placebo-treated dogs (3.8 +/- 1.1 ng/dl, P less than 0.05) while no significant differences were found in F, A, and 17P levels between the two groups. Finally the post-ACTH A/DHA ratio of DOM-treated dogs (1.33 +/- 0.28) was significantly decreased in respect to the placebo-treated animals (5.49 +/- 2.54, P less than 0.01). These data demonstrate that the morphological and functional development of zona reticularis may be subject to dopaminergic control and this could represent an important step in the initiation of adrenarche. However, the cellular mechanism responsible remains to be clarified.

17-alpha-Hydroxyprogesterone↗
PubMed1987

Growth hormone and prolactin secretion after growth hormone-releasing hormone administration, in anorexia nervosa patients, normal controls and tamoxifen-pretreated volunteers.

Anorexia nervosa is associated with several abnormalities in GH secretion elicited by different stimuli. To investigate the precise mechanism of this alteration, GHRH was administered to 14 women: a group of eight anorexia nervosa patients in the acute phase of their illness and a control group of six age-matched volunteers. As patients with anorexia nervosa have chronic low oestrogen values, the volunteer women of the control group underwent a second GHRH test after pretreatment with the oestrogen receptor blocker tamoxifen. GHRH 1-29 (1 microgram/kg i.v.) induced a GH peak (mean +/- SEM) of 28.2 +/- 5.1 ng/ml (GH ng/ml x 2 = mU/l) at 30 min in the anorectic patients. This value was no different from the GHRH-stimulated GH peak in the control women (28.1 +/- 10.0 ng/ml). Tamoxifen pretreated women had a GH peak after GHRH of 35.6 +/- 9.7 ng/ml, not significant versus control test. Compared with the control group, oestrogen levels were significantly lower in anorectic patients and higher in tamoxifen-treated women. GHRH administration induced a small PRL peak at 15 min that was similar in the three groups tested. After this 15 min peak, PRL in both anorexic and tamoxifen-treated women returned toward basal values steadily. However, in untreated control women a second PRL peak was evident at 60 min. In conclusion, GHRH-induced GH secretion in anorexia nervosa patients was similar to that in control subjects and in controls under oestrogen receptor blockade.

Acute Disease↗
PubMed1987

Adrenal cortex and type II polycystic ovary syndrome.

The aim of this study was to investigate whether the adrenal gland participates in the pathogenesis of type II polycystic ovary syndrome (PCO), and, if so, to see if an altered pattern of ACTH secretion might be responsible. Circadian secretion and pulsatility (morning and evening) of ACTH, and adrenal and pituitary responsiveness to exogenous ACTH and GnRH, respectively, were evaluated in 10 women with type II PCO and 10 normally menstruating women. After the patients had been administered oral dexamethasone (0.5 mg each night) for 3 months, studies were repeated. Mean plasma values of PRL, testosterone, DHA-S and 17-OH progesterone (17-P) measured by RIA were significantly higher (p less than 0.05) in patients than in controls. FSH and sex hormone binding globulin (SHBG) were significantly lower (p less than 0.05). Cortisol and 17-P responses to ACTH, and the LH/FSH ratio (both in basal conditions and after GnRH stimulation) were significantly higher (p less than 0.05) in patients. ACTH circadian secretion and pulsatility were similar in both groups. Treatment with dexamethasone significantly reduced plasma values of testosterone, DHA-S, androstenedione (adione), cortisol and the LH/FSH ratio (basal and after GnRH), but adrenal hyperresponsiveness to ACTH was maintained. ACTH pulsatility and secretion were significantly (p less than 0.05) reduced in the morning. Our results suggest that there are abnormalities at the adrenal level in type II PCO. Given that ACTH secretion appears to be normal and that adrenal hyperresponsiveness is still observed after treatment with dexamethasone, it is tempting to speculate that excessive trophic stimulation of the gland by a factor other than ACTH could exist in such patients.

17-alpha-Hydroxyprogesterone↗
PubMed1986

Atropine selectively blocks GHRH-induced GH secretion without altering LH, FSH, TSH, PRL and ACTH/cortisol secretion elicited by their specific hypothalamic releasing factors.

The role of acetylcholine in the regulation of the hypothalamo-pituitary system in man was assessed using atropine, which selectively blocks cholinergic muscarinic receptors. Paired tests were performed in 10 normal men using either GHRH (1 microgram/kg i.v.), or TRH (300 micrograms i.v.) plus LHRH (100 micrograms i.v.) plus corticotrophin releasing hormone (CRH) (1 microgram/kg i.v.) with or without atropine given 30 min previously (1 mg i.m.). The GHRH-induced GH secretory peak (17.8 +/- 3.0 ng/ml) was completely blocked by atropine administration (2.8 +/- 0.6 ng/ml) (P less than 0.05). Atropine did not, however, modify TRH-induced TSH and PRL secretion, nor FSH and LH release induced by the LHRH pulse. ACTH/cortisol secretion elicited by CRH was also unaffected by atropine. These results suggest that atropine blockade of GHRH-induced GH secretion is highly specific, and constitutes an indication of the importance of cholinergic control of GH function. Furthermore, atropine's lack of action on the other pituitary hormones rules out the possibility that it acts non-specifically, i.e. via blood flow changes or toxic effects.

Adrenocorticotropic Hormone↗