Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:040593 (CRH)
 2,662 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of PGE2 on ACTH and cortisol responses to CRH was studied in 6 healthy men who received CRH i.v. during either saline or PGE2 infusions which were started 60 min. before testing. ACTH and cortisol responses to CRH were greater during PGE2 infusion compared to the control study. The results indicate that PGE2 positively modulates CRH-induced ACTH secretion.
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PMID:Role of prostaglandin E2 (PGE2) on the corticotropin-releasing hormone (CRH)-induced ACTH release in healthy men. 132 3

Experimental evidence indicates that arginine vasopressin (AVP) contributes to the release of ACTH under certain conditions. The present study investigates the role of vasopressin as a secretagogue of ACTH during cigarette smoking or nicotine infusion with additional injection of corticotropin releasing hormone (CRH) and using the specific AVP antagonist d(CH2)5Tyr(Me)-AVP. We first tested the effect of the AVP antagonist (10 micrograms/kg body weight i.v.) on ACTH and cortisol release following cigarette smoking in 15 healthy young male smokers. Smoking led to marked increments in plasma nicotine and to a small rise in plasma ACTH and cortisol. Mean plasma ACTH and cortisol levels were at no time significantly altered by the antagonist. This might be due to a slight agonistic effect of the AVP antagonist, to high interindividual variability of the ACTH and cortisol responses after smoking or to a negligible role of AVP in smoking-induced ACTH release. In a second study we performed the following tests in six healthy male non-smokers: (1) nicotine infusion (1.0 micrograms/kg body weight per min); (2) CRH i.v. (100 micrograms); (3) AVP antagonist i.v. (5 micrograms/kg); (4) nicotine infusion plus CRH i.v.; (5) nicotine infusion plus AVP antagonist i.v.; (6) nicotine infusion plus CRH and AVP antagonist i.v.; and (7) sham infusion. Nicotine infusion led to greater increments of AVP, ACTH and cortisol than smoking without causing nausea. Peak nicotine levels after nicotine infusion were lower than after smoking. The AVP antagonist in the reduced dosage given alone had no effect on hormone levels. However, it slightly attenuated the effect of nicotine on ACTH and cortisol (P less than 0.05, ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of vasopressin in the nicotine-induced stimulation of ACTH and cortisol in men. 132 53

Duration and magnitude of hypothalamic-pituitary-adrenal axis suppression caused by daily oral administration of a glucocorticoid was investigated, using an anti-inflammatory dose of prednisone. Twelve healthy adult male dogs were given prednisone orally for 35 days (0.55 mg/kg of body weight, q 12 h), and a control group of 6 dogs was given gelatin capsule vehicle. Plasma cortisol (baseline and 2-hour post-ACTH administration) and plasma ACTH and cortisol (baseline and 30-minutes post corticotropin-releasing hormone [CRH] administration) concentrations were monitored biweekly during and after the 35-day treatment period. Baseline plasma ACTH and cortisol and post-ACTH plasma cortisol concentrations were significantly (P less than 0.05) reduced in treated vs control dogs after 14 days of oral prednisone administration. By day 28, baseline ACTH and cortisol concentrations remained significantly (P less than 0.05) reduced and reserve function was markedly (P less than 0.0001) reduced as evidenced by mean post-CRH ACTH, post-CRH cortisol, and post-ACTH cortisol concentrations in treated vs control dogs. Two weeks after termination of daily prednisone administration, significant difference between group means was not evident in baseline ACTH or cortisol values, post-CRH ACTH or cortisol values, or post-ACTH cortisol values, compared with values in controls. Results indicate complete hypothalamic-pituitary-adrenal axis recovery 2 weeks after oral administration of an anti-inflammatory regimen of prednisone given daily for 5 weeks.
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PMID:Duration of pituitary and adrenocortical suppression after long-term administration of anti-inflammatory doses of prednisone in dogs. 132 43

Maternal plasma progestagen concentrations increase about 20 days before parturition. The major contributors to the increase are reduced metabolites (ie 5 alpha-pregnanes). Precocious increases (ie less than 310 days of gestation) in these metabolites may occur in abnormal pregnancies. The effects of CRH, ACTH or betamethasone administered to the foetus at gestational ages ranging from about 250 to 320 days were examined. Sixteen healthy pony mares were used for foetal injection employing aseptic techniques. Water or normal saline were used as controls. Maternal plasma progestagen concentrations were measured using a commercial radioimmunoassay (RIA) progesterone kit and results were confirmed using gas chromatography-mass spectrometry (GC-MS). Results demonstrated clearly that an increase in maternal plasma progestagen concentrations occurred after injection of ACTH, CRH or betamethasone to the foetus, irrespective of gestational age. A comparable increase was not observed in the control animals. Of the 16 mares in which the foetus was injected, 13 produced viable foals at gestational ages ranging from 307 to 339 days whereas 3 mares delivered non-viable foals at 284 to 306 days gestation. The results support the hypothesis that the pre-parturient rise in progestagens occurring in the mare is the result of foetal adrenocortical activity.
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PMID:Increase in plasma progestagen concentrations in the mare after foetal injection with CRH, ACTH or betamethasone in late gestation. 139 5

It is known that glucocorticoids can influence anterior pituitary hormones other than ACTH. Their effects on the hypothalamic-pituitary-thyroid axis are controversial. To further investigate this issue, the acute and chronic effects of high plasma cortisol levels on TSH secretion were evaluated in 20 normal subjects and in 14 patients with Cushing's syndrome. In normals, high plasma cortisol levels were obtained by giving ACTH 250 micrograms or CRH 100 micrograms iv as a bolus or by an hydrocortisone 500 mg infusion over 1 h. Acute cortisol increase produced no effect both on basal and TRH-stimulated TSH secretion. In patients with Cushing's syndrome, basal TSH levels, low or suppressed, showed an impaired response to TRH, inversely correlated with urinary cortisol values. After successful surgery, TSH and its response to TRH became normal in concomitance with the normalization of plasma and urinary cortisol levels. Our data show the lack of an acute inhibitory effect of high plasma cortisol levels on TRH-TSH axis. However, after long-term exposure to high plasma cortisol levels, i.e. Cushing's syndrome, inhibition of both basal and TRH-stimulated TSH secretion was demonstrated. These findings indicate that only prolonged hypercortisolism does interfere with pituitary TSH secretion. The underlying mechanisms are still unclear.
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PMID:Acute and chronic effects of high glucocorticoid levels on hypothalamic-pituitary-thyroid axis in man. 132 49

Up to now, the diagnosis of silent corticotroph cell pituitary adenomas has been made only on histopathological basis. In this paper we describe 6 women affected with pituitary adenomas, without evident clinical features of hypercortisolism, in whom retrospective data suggested the possibility of clinically diagnosing silent corticotropinomas in vivo. In all patients basal ACTH and cortisol levels were normal, and the low-dose dexamethasone test constantly suppressed serum cortisol and urinary 17-hydroxycorticosteroid levels. The CRH and/or lysine-vasopressin tests, performed in five patients, always induced exaggerated ACTH/cortisol rises. In three cases the response to the opiate agonist loperamide was assessed and no inhibition of ACTH/cortisol levels was found. All patients underwent pituitary surgery. In five cases evidence of corticotropinoma was obtained by immunohistochemistry or immunofluorescence studies; moreover, in one adenoma ACTH was secreted into the culture medium, and in another one CRH and arginine-vasopressin induced a marked intracellular [Ca++] rise. Electron microscopy study of the adenoma, removed from three patients, showed the presence of adenomatous corticotroph cells. Finally, in another woman no hormonal abnormalities were initially observed and she was operated for a "nonfunctioning" pituitary adenoma, but four years later an overt Cushing's disease appeared, suggesting that a silent corticotropinoma subsequently became functional, although the formation of a different adenoma cannot be excluded. In conclusion, the occurrence of ACTH/cortisol hyperresponsiveness to CRH and/or lysine-vasopressin and the lack of suppression of ACTH/cortisol secretion to opioid agonists in patients with apparently "nonfunctioning" pituitary tumors might allow the in vivo recognition of silent corticotropinomas.
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PMID:The silent corticotropinoma: is clinical diagnosis possible? 132 50

Utilizing push-pull perfusion, we examined the effects of intravenous (iv) administration of human recombinant tumor necrosis factor (TNF)-alpha on the levels of plasma adrenocorticotropin (ACTH) and corticotropin releasing hormone (CRH) in the median eminence (ME) of freely moving male rats. The ME was perfused with artificial cerebrospinal fluid between 11:00 and 14:00 h, and perfusates and blood samples were collected every 20 min. TNF-alpha (1.0 microgram), but not vehicle only, given as an iv bolus at 12:00 h significantly stimulated both plasma ACTH and ME-CRH. The increase in ME-CRH clearly preceded that of plasma ACTH. This is the first to characterize the temporal profile of CRH secretion in the ME after iv administration of TNF-alpha to freely moving rats. These in vivo data strongly suggest that TNF-alpha stimulates ACTH secretion, at least in part, by triggering hypothalamic CRH release. In addition, combined with our previous data obtained by iv administration of human recombinant interleukin-1 under the same experimental condition, the present study also suggests that iv injected TNF-alpha and interleukin-1 may share a common site of action in the brain, such as the ME, to stimulate CRH secretion.
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PMID:Intravenous administration of tumor necrosis factor-alpha stimulates corticotropin releasing hormone secretion in the push-pull cannulated median eminence of freely moving rats. 132 21

Bacterial lipopolysaccharide (LPS) stimulates the hypothalamo-pituitary-adrenal axis by a mechanism involving the release of cytokines, which activate the CRH-ACTH system and, as a result, increase glucocorticoid secretion. In the present study we investigated the possibility that endogenous sex hormones modulate the in vivo endotoxin-stimulated adrenal and immune responses in adult BALB/c mice. In preliminary experiments we determined that the maximal glucocorticoid release in response to LPS (50 micrograms, ip) administration was reached 2 h after treatment. The endotoxin effect on the adrenal and immune responses was then tested in male, randomly cycling female, 20-day-gonadectomized and 20-day-gonadectomized mice treated with either testosterone or estradiol. In addition, in vitro experiments were performed to determine whether 1) LPS exerts any direct effect on basal and ACTH-stimulated corticosterone release, and 2) adrenal function is influenced by bilateral gonadectomy and sex steroid therapy. Our results indicate that 1) randomly cycling female mice have significantly more pronounced corticosterone secretion than males 2 h after endotoxin injection, although the tumor necrosis factor responses were similar; 2) the response of the hypothalamo-pituitary-adrenal axis to endotoxin stimulation in female mice was invariable throughout the different stages of the normal estrous cycle; 3) gonadectomy leads to enhanced (P < 0.05) adrenal and immune responses to LPS stimulation compared to the responses in shams; 4) the endotoxin-elicited adrenal and immune overresponses observed in gonadectomized mice are reversed by testosterone treatment, regardless of sex; 5) LPS does not directly modify spontaneous and ACTH-stimulated adrenal corticosterone secretion; and 6) gonadectomy alone or combined with sex steroid therapy does not increase the in vitro adrenal response to ACTH stimulation. Our findings further suggest an evident neuroendocrine-immunological sexual dimorphism during the acute phase of inflammatory processes.
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PMID:Effects of gonadectomy and sex hormone therapy on the endotoxin-stimulated hypothalamo-pituitary-adrenal axis: evidence for a neuroendocrine-immunological sexual dimorphism. 133 May 1

There is still some controversy concerning the question of whether Cushing's disease in man is caused by a primary dysfunction of the pituitary or a hypothalamic disorder. In the latter option, excessive hypothalamic stimulation of pituitary corticotropes would cause or contribute to the genesis of POMC-secreting adenomas. In the present study cerebrospinal fluid (CSF) CRH levels and levels of ACTH and cortisol in CSF and plasma were measured in clinically healthy dogs, in dogs with pituitary-dependent hyperadrenocorticism (PDH), and in dogs with hyperadrenocorticism due to an adrenocortical tumor (ATH). In CSF from dogs with PDH, CRH concentrations (226.6 +/- 14.4 ng/liter) were significantly (P < 0.05) lower than those in control dogs (309.5 +/- 20.3 ng/liter). In the dogs with ATH, CSF CRH concentrations (211.0 +/- 40.3 ng/liter) were in the range of those in PDH dogs. In dogs with ATH, CSF ACTH levels (13.0 +/- 3.0 ng/liter) were significantly (P < 0.05) lower than those in control dogs (63.4 +/- 3.5 ng/liter), whereas in dogs with PDH, the levels (116.8 +/- 47.5 ng/liter) were not different from those in the control group. In control dogs, the concentrations of CSF CRH and plasma ACTH were significantly correlated (r = 0.635; P < 0.01). This functional dependency appeared to be disturbed in dogs with PDH, as in these dogs CSF CRH concentrations did not correlate with plasma ACTH concentrations. It is concluded that continuous hyperstimulation of pituitary corticotropes with hypothalamic CRH is probably not the cause of excessive ACTH secretion in dogs with pituitary-dependent hyperadrenocorticism.
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PMID:Corticotropin-releasing hormone and adrenocorticotropic hormone concentrations in cerebrospinal fluid of dogs with pituitary-dependent hyperadrenocorticism. 133 44

Rat GH-releasing hormone (GHRH), mainly contained in hypothalamic neurons, has also been identified in several extraneural tissues, including the gastrointestinal tract, placenta, ovary, and testis. In the testis, GHRH mRNA is ontogenically regulated, and GHRH immunoreactivity can be observed in interstitial cells and tubules, suggesting an intratesticular role for the peptide. Leydig cells in culture are able to produce hypothalamic releasing hormones, i.e. CRH, which acts as an autocrine negative regulator of Leydig cell function. In this study we investigated whether GHRH is present in Leydig cells and evaluated the role of the peptide in Leydig cell function. Adult Leydig cells in culture produced considerable amounts of immunoreactive GHRH [23.9 +/- 2.1 (+/- SE) pg/10(6) cells.30 min], and the release of the peptide was acutely stimulated by hCG. HPLC analysis of GHRH in media from basal and hCG-treated cultures showed the presence of a single peak eluting at the same retention time as that of hypothalamic rat GHRH. Radioligand binding and activation studies revealed a common receptor for vasoactive intestinal peptide (VIP) and rat GHRH in Leydig cell membrane. Specific binding of [125I]VIP to Leydig cell membranes showed the presence of a single site, with high affinity and low binding capacity. The relative potencies of VIP-related peptides for inhibition of radioligand binding were: VIP > rat GHRH > secretin > human GHRH. In cultured Leydig cells, GHRH and VIP stimulated cAMP production, consistent with coupling of the receptor to the adenylate cyclase system. VIP displayed a lower ED50 than GHRH in stimulating cAMP production (P < 0.01), comparable with the higher binding potency of this peptide. No additive effects of VIP- and GHRH-stimulated cAMP generation were observed, suggesting that both peptides compete for the same receptor protein. GHRH and VIP had no effect on basal steroidogenesis, indicating a lack of tonic actions and compartmentalization of the peptides' effect. On the other hand, GHRH acted as a potentiator of the acute gonadotropin stimulation of testosterone production and cAMP generation. [125I]hCG binding to the Leydig cells in culture showed that GHRH was unable to affect the number or affinity of binding sites for hCG, indicating that the GHRH-sensitizing effect on LH action is beyond the level of gonadotropin binding and possibly is through the facilitation of LH receptor coupling functions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Growth hormone-releasing hormone is produced by rat Leydig cell in culture and acts as a positive regulator of Leydig cell function. 133 49


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