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)

Isolated adrenocorticotropin deficiencies are rare. Two cases are reported, one, with hypoglycaemia, the other with weakness and hypotension, with a review of the published cases during the past twenty years. The adrenal defect impairs severely the glucocorticoid secretion while aldosteron is normal. Tetracosactid stimulates adrenal secretion. ACTH activity measurable in serum is very low and not affected by metyrapone. Other pituitary secretions are normal. The hypothalamic or pituitary level of the defect will be situated when CRH test available.
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PMID:[Adrenal insufficiencies caused by isolated corticotropic deficiency. 2 cases]. 18 90

The effects of oral administration of 100 mg per kg per day cyproterone acetate (CPA) for four weeks on cells of the pars distalis, as revealed by the immunoperoxidase technique and chemical staining, were studied in the ovariectomized beagle bitch. For immunochemical staining antisera to the following hormones were used: canine GH, canine PRL, procine ACHT, bovine TSH beta, bovine LH beta and human FSH beta1. The most striking effects of the treatment were an overall increase in the relative proportion of GH cells and a marked morphological indication of high secretory activity in these cells. In contrast, PRL cells were not affected significantly. In all ovariectomized control bitches a marked atrophy of the cells stained for FSH beta (FSH cells) and hypertrophy of the cells shown to contain LH beta (LH cells) were observed. FSH cells became enlarged, while LH cells appeared reduced in size by administration of CPA. In some treated bitches ACTH/MSH cells showed atrophy and regressive changes, whereas TSH cells seemed to become enlarged and were more densely arranged. These structural responses indicate that, in addition to its partial antigonadotropic properties, CPA as a synthetic progesterone derivative may stimulate GH secretion and possibly suppress CRH-ACTH activity in the ovariectomized beagle bitch.
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PMID:Effect of cyproterone acetate on cells of the pars distalis of the adenohypophysis in the beagle bitch. 20 Mar 63

1. The effects of stress, adrenalectomy and corticosterone treatment on the functional activity of the hypothalamo-pituitary-adrenocortical system have been studied using highly sensitive and precise bio-assay methods for the determination of ACTH and CRH.2. Adrenalectomy resulted in a rise and corticosterone treatment a fall in the hypothalamic CRH content and the plasma ACTH concentration.3. Stress caused a fall followed by a rise in the hypothalamic CRH content, a rise in the pituitary and plasma ACTH concentrations and an increase in the plasma corticosterone concentration.4. The stress-induced changes in hypothalamic CRH content and pituitary and plasma ACTH were exaggerated in adrenalectomized rats but normal in adrenalectomized rats treated with corticosterone. They were also normal in animals injected I.P. with corticosterone 15 min before the stress but inhibited in those similarly treated 60 min previously.5. The ability of adenohypophyses and hypothalami to synthesize and release in vitro ACTH and CRH respectively in response to trophic stimuli was exaggerated in glands removed from adrenalectomized rats and reduced in those removed from corticosterone-treated rats.6. Addition of corticosterone to the pre-incubation medium reduced the capacities of adenohypophyses and hypothalami removed from untreated rats to synthesize and release ACTH and CRH respectively.
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PMID:The influence of corticosteroids on the secretion of corticotrophin and its hypothalamic releasing hormone. 22 Apr 13

Two behaviorally active hormones of the pituitary-adrenal system are adrenocorticotropic hormones (ACTH) and corticosterone, and their behavioral effects are facilitation and inhibition of performance of previously learned avoidance responses, respectively. Their uptake, distribution and effects on central nervous system are reviewed. Hypothalamic neurotransmitter control of corticotropin releasing hormone (CRH) is described together with hypothalamic and extra-hypothalamic (hippocampal) regulation of pituitary-adrenal activity. Extra-hypothalamic mediation of the behavioral effects of ACTH is evaluated. Recent isotopic mappings of the efferents of the hippocampal formation have identified pathways from hippocampal subiculum to hypothalamus and posterior lateral and anterior thalamic nuclei. The evidence reviewed suggests a complex circuit involving hippocampal subiculum, thalamus and hypothalamus may be involved both in regulating pituitary-adrenal responses to stress and in mediating the effects of ACTH on avoidance behavior.
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PMID:Central mediation of hormonal influences on instrumental avoidance conditioning. 23 11

For the assessment of hypothalamic corticotropin releasing hormone (CRH) secretory function, insulin test, lysinevasopressin test, and rapid ACTH test were performed and plasma crotisol was assayed. Disturbances of CRH secretory activities were found not to be related with the degree of suprasellar extension of tumors, contents of tumors, the degree of visual disturbances, or the duration of symptoms, and it was supposed that more complex mechanisms were responsible for CRH secretory abnormalities.
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PMID:Hypothalamo-pituitary-adrenal function in pituitary adenoma and craniopharyngioma. Part II: insulin test and clinical features. 30 53

Specific neuroendocrine regulatory mechanisms in rats and mice are known to be involved in the development of pituitary tumours (prolactinomas) in systemic tolerance and carcinogenicity studies of oestrogens, certain progestagens and their combinations. However, the susceptibility of the strain used seems to be of decisive importance. High doses of oestrogens may also, in special cases, stimulate development of PRL cell hyperplasia and tumours in humans. In other species such as the hamster long-term treatment with oestrogens results in hyperplastic and neoplastic changes in MSH-producing cells of the pars intermedia of the pituitary gland. On the other hand, in the dog and monkey, steroid-related pituitary tumours were not observed, in spite of long-term treatment with high doses of oestrogens, progestagens and their combinations. The capability of certain progestagens to stimulate canine GH secretion seems to play a major role as mediator of the species-specific progestagen-induced changes (mammary tumours, diabetes- and acromegalic-like syndrome) in the beagle dog. These progestagens also seem to have, in addition to their antigonadotrophic properties, an inhibitory effect on CRH-ACTH and TRH-TSH activity in the beagle bitch. These effects can be demonstrated in both the hypothalamic-pituitary system and in the corresponding peripheral target organs. These findings in the dog were not comparable to the situation in other species including man. The extent to which all these results in different species are applicable to other species depends on whether their neuroendocrine control systems are qualitatively and/or quantitatively similar. The physiological significance of the different pituitary hormones, sensitivity of target organs as well as a certain genetic disposition in the different species should also be considered. All these factors can vary from species to species. From these facts, it can be easily appreciated that results of experiments on different species with a substance possessing the same quality of biological effect in these species (e.g., oestrogen, progestagen, etc.) can only be compared when the experimental procedure takes account of the effect of this substance on the neuroendocrine system of the different species, and when dosage, mode of administration and period of treatment are correspondingly matched to the physiological conditions of each species.
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PMID:Evaluation of effects of sexual steroids on the hypothalamic-pituitary system of animals and man. 38 May 19

The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects. Plasma catecholamine and PP levels rose in both groups in response to hypoglycemia and the secretory response of ACTH was lower in the diabetic subjects (p < 0.01). GRP concentrations increased during hypoglycaemia (p < 0.01) while a reduction in AVP occurred at the start of hypoglycaemia (p < 0.001). The plasma AVP concentrations were higher in the diabetic group compared with those in the normal group (p < 0.05). The NPY concentrations were higher in the normal subjects (p < 0.05) but no change in the mean level occurred in either group during hypoglycaemia. No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH. These observations support the view that regulatory peptides, if involved in glucose homeostasis, may rather have a modulatory effect than a direct action in restoring normoglycaemia.
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PMID:The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent) diabetes mellitus and in normal man. 128 60

The risk for depression increases at two opposite times of the year--late spring/early summer and late fall/early winter. In 15% of patients with recurrent major depression, depressive episodes regularly recur on an annual basis in one of the two seasonal risk periods. Thus, there are primarily two forms of seasonal affective disorder: recurrent fall-winter depression and recurrent spring-summer depression. The opposite seasonal types of depression tend to have opposite vegetative symptoms. Sleep, appetite and weight increase in winter depression and decrease in summer depression. An important implication of the seasonality of depression is that some type of depression may be caused by changes in the physical environment and that manipulations of the physical environment may be used as treatments. There is now extensive evidence that exposure to bright artificial light is an effective treatment of recurrent winter depression. A corollary is that seasonal deficiency of natural light probably induces winter depression. There have been considerable efforts to elucidate the biological mechanisms of winter depression and its response to phototherapy. Although no single system has been shown to be responsible for the syndrome, there is evidence that the indole hormone melatonin, the indole neurotransmitter serotonin, and the peptide neurohormone corticotropin releasing hormone (CRH) play roles in the pathophysiology and phototherapy of winter depression.
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PMID:Seasonal vulnerability to depression. Implications for etiology and treatment. 130 42

21-Hydroxylase congenital adrenal hyperplasia (21-OHCAH) involves a primary defect of the adrenal gland and a secondary involvement of ACTH secretion. The responses of the pituitary-adrenal axis to ovine CRH (oCRH, 1 micrograms/kg) were examined in subjects with different degrees of 21-OH deficiency. We studied 43 subjects: 7 classical and 6 nonclassical (NC) 21-OHCAH patients, 15 heterozygotes (HT) and 15 control subjects. Baseline plasma ACTH levels were higher in classical CAH than in NC-CAH, HT, and control subjects (mean +/- SEM, 66 +/- 14, 6 +/- 1.6, 4 +/- 0.5, and 5 +/- 0.5 pmol/L, respectively). The mean plasma ACTH response to oCRH in NC-CAH (17 +/- 3 pmol/L) was higher than in controls and HT (9 +/- 0.8 and 11 +/- 1.5 pmol/L). The highest ACTH responses to oCRH were obtained for classical CAH patients (126 +/- 29 pmol/L). Plasma cortisol rose after oCRH in control, HT, and NC-CAH patients but did not change in classical CAH. After oCRH, plasma 17-hydroxyprogesterone (17-OHP) were 4 +/- 0.5, 8 +/- 1.6, 93 +/- 28, and 359 +/- 110 nmol/L for controls, HT, NC-CAH, and classical patients, respectively. There was a significant correlation (r = 0.70) between 17-OHP and the ACTH responses to oCRH. The 17-OHP responses to oCRH were also correlated (r = 0.94) with the 17-OHP responses to the synthetic ACTH test. We conclude that the release of endogenous ACTH by oCRH result in graded 17-OHP responses on 21-OH deficiency. The present study also suggests that different degrees of adrenal biosynthetic defect may result in graded ACTH responses to oCRH.
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PMID:Pituitary-adrenal responses to corticotropin-releasing hormone in different degrees of adrenal 21-hydroxylase deficiency. 130 66

Carbamazepine (CBZ) is a widely used therapeutic agent in seizure, pain, and mood disorders. Although CBZ has been shown to inhibit hypothalamic CRH secretion in vitro, limited data suggest that systemic CBZ induces pituitary-adrenal activation. Few data are available to reconcile these effects or clarify their mechanism(s), particularly in healthy human subjects. We report here a study of basal ACTH and cortisol secretion and their responses to ovine CRH administration in nine healthy volunteers, studied both during repeated (2-3 weeks) administration of CBZ and while medication free. CBZ significantly increased mean 24-h urinary free cortisol (mean +/- SE, 197 +/- 17 vs. 137 +/- 24 nmol/day; P less than 0.02) and evening basal total plasma cortisol (113 +/- 17 vs. 83 +/- 14 nmol/L; P less than 0.05) as well as cortisol-binding globulin-binding capacity (497 +/- 36 vs. 433 +/- 28 nmol/L; P less than 0.01). Despite the CBZ-induced hypercortisolism, plasma ACTH responses to CRH during CBZ treatment remained robust, rather than being suppressed by basal hypercortisolism. In fact, during CBZ treatment, we noted a positive correlation between the increase in basal plasma cortisol and the increase in the plasma ACTH response to CRH (r = 0.65; P less than 0.05). We also observed a reduction in cortisol-binding globulin-binding capacity after CRH administration (315 +/- 25 vs. 433 +/- 28 nmol/L; P less than 0.001), which was accentuated by CBZ treatment (342 +/- 19 vs. 497 +/- 36 nmol/L; P less than 0.001; magnitude of fall, -155 +/- 22 nmol/L on CBZ vs. -118 +/- 11 nmol/L off CBZ; P less than 0.05). We conclude that CBZ increases plasma cortisol secretion in healthy volunteers independent of its effect on plasma cortisol-binding capacity. This pituitary-adrenal activation seems to reflect a pituitary, rather than a hypothalamic, effect of CBZ. Hence, despite CBZ-induced hypercortisolism, the ACTH response to CRH remained robust in direct proportion to the CBZ-induced rise in basal plasma cortisol. Thus, we propose that the increased cortisol secretion observed during CBZ treatment reflects a relative inefficacy of glucocorticoid negative feedback at the pituitary. This pituitary-driven increase in cortisol secretion combined with the expected reduction in centrally directed CRH secretion could contribute to the anticonvulsant properties of CBZ.
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PMID:Effects of carbamazepine on pituitary-adrenal function in healthy volunteers. 130 36


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