Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atopic eczema is a chronic inflammatory skin disease which shares some psychological and neuroendocrine disturbances with patients suffering from depression. In view of recent findings of an attenuated response of the hypothalamic-pituitary-adrenal (HPA) system in patients with atopic eczema during a human corticotropin-releasing hormone (hCRH) challenge paradigm fourteen consecutive non-specifically trained in-patients with atopic eczema (8 men, 6 women) and an age-matched control group (8 men, 6 women) performed exhausting incremental graded bicycle exercise to evaluate cortisol, adrenocorticotropin (ACTH), beta-endorphin, epinephrine and norepinephrine releases induced by physical stress. The exercise yielded significant increases in cortisol, ACTH, beta-endorphin, epinephrine and norepinephrine concentrations in both groups. Patients with severe eczema displayed a significantly lower increase in norepinephrine levels when compared with the less affected patient group. In contrast to the challenge with exogenous hCRH no substantial difference in the net responses of ACTH and cortisol could be detected between patients with atopic eczema and controls using the physical stress paradigm. These substantial differences in the net outcome between both challenges may be related to the potential synergizing effects of various neuropeptides, e.g. CRH and vasopressin, when activating the HPA system by challenges at a suprapituitary site which may override subtle disturbances in the responsivity of the HPA system as revealed by CRH challenge alone in patients with atopic eczema.
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PMID:Physical stress-induced secretion of adrenal and pituitary hormones in patients with atopic eczema compared with normal controls. 908 93

The objective of the present study was to examine the effect of changes in plasma osmolality (pOsm) on the responses of the pituitary-adrenal axis to CRH and atrial natriuretic peptide (ANP) release in patients with central diabetes insipidus (DI). Eight normal subjects and six DI patients were subjected to human CRH (hCRH) (1 microgram/kg) stimulation alone or associated with isotonic volume loading (0.9% NaCl, 12 mL.kg.60 min) or an osmotic stimulus (5% NaCl, 0.06 mL.kg/min.120 min). The DI group showed significantly increased pOsm and undetectable or low plasma arginine vasopressin (AVP) during all tests. In the control group, pOsm and plasma AVP increased only during the osmotic stimulus. The DI group presented lower plasma ANP levels than controls during osmotic stimulus and isotonic volume loading. The lower ANP secretion in DI patients corroborates the importance of neurohypophyseal hormones in ANP regulation. Basal plasma ACTH and cortisol levels did not differ between controls and DI. The latter group presented a higher ACTH response than controls during stimulation with hCRH alone [area under the curve (AUC) 1138 +/- 99 vs. 709 +/- 62 pmol.L/min] and hCRH/5% NaCl (AUC 1602 +/- 209 vs. 1158 +/- 187 pmol.L.min). The DI cortisol AUC were higher than controls during stimulation with hCRH alone (65,471 +/- 6,070 vs. 48,062 +/- 3,476 nmol.L.min) and hCRH/5% NaCl (89,005 +/- 10,043 vs. 62,105 +/- 5,600 nmol.L.min). The highest ACTH and cortisol responses to hCRH in both groups were obtained with hCRH/5% NaCl. There was a significant correlation between mean pOsm and ACTH response to hCRH (r = 0.62). The increased responses to hCRH with increasing pOsm were present in control subjects and in patients with DI. However, at any given level of pOsm, there was no difference in ACTH response between controls and DI. These data indicate that the acute increases in pOsm augmented the ACTH and cortisol responses to hCRH that involve other factors besides magnocellular AVP.
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PMID:Effect of plasma osmolality on pituitary-adrenal responses to corticotropin-releasing hormone and atrial natriuretic peptide changes in central diabetes insipidus. 910 Jun 2

Although the effects of the various secretagogues on corticotropin (ACTH) secretion have been well studied, their effects on the POMC gene expression have not been thoroughly characterized. In this study, we established a new model system using the AtT20 mouse corticotroph tumor cell line transfected stably with a plasmid containing 0.7 kb of the rat POMC 5' promoter-luciferase fusion gene. The responsiveness to exogenous CRH improved markedly when the cells were cultured with low serum medium (1% FBS) compared with serum rich medium (10%). Using this culture condition, we examined the effects of not only CRH but also other secretagogues such as catecholamines, vasopressin, and angiotensin II, upon the transcriptional activity of the POMC gene. CRH stimulated POMC promoter activity (3.5-fold increase) as well as cAMP generation and ACTH secretion in a dose- and time-dependent manner, with the maximal effect being observed 3-5 h after the start of incubation. Catecholamines, especially epinephrine (10 nM and above), also stimulated all parameters, although less potently than CRH, and the effect was mimicked by the beta-, but not alpha-adrenergic, agonist, suggesting the involvement of the beta-adrenergic receptor. The combined effects of epinephrine and CRH were greater in all parameters than those of CRH alone, and the effects of both hormones were completely blocked by H89, an inhibitor of protein kinase A. Vasopressin and angiotensin II showed minimal effects on POMC expression. Our results suggest that 1) catecholamines, as well as CRH, positively regulate the POMC gene at physiological concentrations; 2) the cAMP-PKA system is the common intracellular signaling pathway for CRH and catecholamines; and 3) vasopressin and angiotensin II also have weak but significant stimulatory effects on POMC promoter activity.
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PMID:Regulation of the rat proopiomelanocortin gene expression in AtT-20 cells. I: Effects of the common secretagogues. 911 88

Arginine-vasopressin (AVP) is a hypothalamic hormone that, like CRH, stimulates the pituitary release of ACTH, thereby activating adrenal glucocorticoid secretion. Evidence indicates that rat adrenal medulla contains a CRH-ACTH system duplicating that existing at the hypothalamo-pituitary level and involved in the paracrine stimulation of the cortex secretion. Therefore, we investigated by RIA the effect of AVP on the release of CRH and ACTH immunoreactivities (IR) by rat adrenal medulla in vitro. AVP concentration-dependently enhanced the release of both CRH-IR and ACTH-IR, and the effect was blocked by a selective antagonist of the V1 subtype of AVP receptors. The CRH receptor antagonist alpha-helical-CRH partially reversed AVP-evoked rise in ACTH-IR release, without altering either CRH response or basal secretions of CRH and ACTH. The specific inhibitors of protein kinase C Ro31-8220 and calphostin C abolished both CRH and ACTH responses to AVP. In conclusion, our present findings suggest that AVP stimulates intramedullary the CRH-ACTH system, acting via V1 receptors and activating protein kinase C.
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PMID:Arginine-vasopressin stimulates CRH and ACTH release by rat adrenal medulla, acting via the V1 receptor subtype and a protein kinase C-dependent pathway. 914 90

A 40-year-old woman with adrenal insufficiency was clinically diagnosed and examined with human corticotropin releasing hormone (CRH). This patient with secondary hypo-adrenalism has shown a normal serum cortisol response to exogenous ACTH administration and has been examined with CRH, lysine-vasopressin (LVP) and insulin tolerance test (ITT), respectively. Success in secreting ACTH in response to both CRH and LVP tests, but not ITT, suggests that this disorder was possibly due to a hypothalamic CRH deficiency rather than pituitary corticotroph dysfunction. A combination of the CRH test and ITT has come to play an increasingly significant role in the diagnosis and differential diagnosis of isolated ACTH deficiency syndrome.
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PMID:A case of adrenal insufficiency due to acquired hypothalamic CRH deficiency. 915 24

Pituitary corticotropic cells express a specific vasopressin receptor, called V1b or V3, through which vasopressin stimulates corticotropin secretion. We recently cloned a cDNA coding for this receptor and showed that it belongs to the G protein-coupled receptor family. V3 mRNA is readily detected by RT-PCR in normal human pituitaries and corticotropic pituitary adenomas but not in PRL or GH-secreting adenomas, thus demonstrating that, like POMC itself and the CRH receptor, V3 is a marker of the corticotropic phenotype. Nuclease protection experiments suggest that V3 is overexpressed in some corticotropic adenomas, and thus may play a role in tumor development by activating the phospholipase C-signalling pathway. In addition analysis of its expression in nonpituitary neuroendocrine tumors showed a striking association with carcinoids of the lung responsible for the ectopic ACTH syndrome.
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PMID:V3 vasopressin receptor and corticotropic phenotype in pituitary and nonpituitary tumors. 916 61

Recent work has demonstrated that the brain has the capacity to synthesize impressive amounts of the gases nitric oxide (NO) and carbon monoxide (CO). There is growing evidence that these gaseous molecules function as novel neural messengers in the brain. This article reviews the pertinent literature concerning the putative role of NO and CO as critical neurotransmitters and biological mediators of the neuroendocrine axis. Abundant evidence is presented which suggests that NO has an important role in the control of reproduction due to its ability to control GnRH secretion from the hypothalamus. NO potently stimulates GnRH secretion and also appears to mediate the action of one of the major transmitters controlling GnRH secretion, glutamate. Evidence is presented which suggests that NO stimulates GnRH release due to its ability to modulate the heme-containing enzyme, guanylate cyclase, which leads to enhanced production of the second messenger molecule, cGMP. A physiological role for NO in the preovulatory LH surge was also evidenced by findings that inhibitors and antisense oligonucleotides to nitric oxide synthase (NOS) attenuate the steroid-induced and preovulatory LH surge. CO may also play a role in stimulating GnRH secretion as heme molecules stimulate GnRH release in vitro, an effect which requires heme oxygenase activity and is blocked by the gaseous scavenger molecule, hemoglobin. Evidence is also reviewed which suggests that NO acts to restrain the hypothalamic-pituitary-adrenal (HPA) axis, as it inhibits HPA stimulation by various stimulants such as interleukin-1 beta, vasopressin, and inflammation. This effect fits a proinflammatory role of NO as it leads to suppression of the release of the anti-inflammatory corticosteroids from the adrenal. Although not as intensely studied as NO, CO has been shown to suppress stimulated CRH release and may also function to restrain the HPA axis. Evidence implicating NO in the control of prolactin and growth hormone secretion is also reviewed and discussed, as is the possible role of NO acting directly at the anterior pituitary. Taken as a whole, the current data suggest that the diffusible gases, NO and CO, act as novel transmitters in the neuroendocrine axis and mediate a variety of important neuroendocrine functions.
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PMID:Gaseous transmitters and neuroendocrine regulation. 920

During the first half of nocturnal sleep, the secretory response of the pituitary-adrenal axis to either CRH or vasopressin (VP) administration is reduced. Two experiments were performed aiming (i) to investigate the impact of sleep on the response to a combined CRH/VP administration and (ii) to specify the onset of sleep associated pituitary-adrenal suppression and its relation to specific sleep stages. In experiment I, we compared the effect of simultaneous administration of VP (0.5 IU i.v., within 6 min) and CRH (50 micrograms bolus i.v., in the third min of VP infusion) on the secretion of ACTH, cortisol and GH in healthy men during the first nocturnal epoch of slow wave sleep (SWS) and during nocturnal wakefulness. The increase of ACTH and cortisol concentrations after combined VP/CRH administration was distinctly higher during wakefulness than sleep (P < 0.01). In experiment II, CRH (30 micrograms/h, after an initial bolus of 30 micrograms) was continuously infused in 7 healthy men on 2 nights. On one of the nights, the men were allowed to sleep (between 23.00 h and 05.00 h) after a 3-h period of wakefulness, on the other night they stayed awake throughout the experiment. In both conditions, CRH enhanced ACTH/cortisol plasma levels. Compared with concentrations during continuous wakefulness, sleep and in particular SWS was associated with a suppression of ACTH/cortisol levels (P < 0.05). The findings further support an inhibitory influence of early nocturnal sleep on pituitary-adrenal activity. The effect appears to be strongest during SWS and is probably mediated via hypothalamic secretion of a release inhibiting factor of ACTH.
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PMID:Slow wave sleep drives inhibition of pituitary-adrenal secretion in humans. 922 58

Antisense oligodeoxynucleotides (ODN) offer the potential advantage to manipulate neuropeptide or neuropeptide receptor expression within the brain transiently and site-specifically, thus providing a tool for neuroendocrinological research into the physiological function of a particular neuropeptide system. In this study, various approaches are introduced which reveal that antisense ODN may exert acute, short-term effects on neuronal responsiveness to afferent stimuli, as well as long-term effects on neuropeptide/receptor protein availability in a given system depending on the duration of treatment. Short-term effects were seen in that oxytocin (OXT) and vasopressin (AVP) antisense ODN affected electrophysiological and secretory parameters of oxytocinergic and vasopressinergic neurons, respectively, as well as their ability to express the Fos protein in response to afferent stimulation a few hours after a single infusion into the hypothalamic supraoptic nucleus. In this study, two methodological approaches to study long-term effects of the antisense ODN are exemplified, in which antisense ODN directed against the mRNA coding for the neuropeptide itself or its receptor were used. The repeated infusion of corticotropin releasing hormone (CRH) antisense ODN into the paraventricular nucleus resulted in reduced immunoreactive CRH, but not AVP, in the external zone of the median eminence. Furthermore, in order to evaluate the receptor-mediated effects of CRH and AVP released locally within the paraventricular nucleus on adrenocorticotropin (ACTH) release from the pituitary, CRH receptor (and also AVP receptor) antisense ODN were repeatedly infused into the hypothalamic nuclei; this treatment resulted in an elevation of stimulated, but not basal, ACTH release into the blood. However, in addition to these obvious antisense effects, results are discussed which demonstrate sequence-unspecific effects of phosphorothioated ODN, suggesting that some of their mechanisms of action are not yet understood.
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PMID:Antisense oligonucleotides in neuroendocrinology: enthusiasm and frustration. 924 79

In a brief review of advances in endocrinology in the last two years the author discusses above all the vain expectations of a drug against obesity-the adipose tissue hormone leptin. Its elevated blood level in human obesity indicates that its secretion depends on the mass of adipose tissue and it is not certain whether leptin reduces the food intake in humans. Perhaps resistance to leptin is involved. New receptor diseases were revealed: mutation of LH receptors leads in both sexes to hypogonadism. Mutation of the calcium receptor in parathyroid cells leads to familial hypocalciuric hypercalcaemia or autosomal dominant hypocalcaemia. The complex regulation of the tonus of the vascular wall by endothelins is still the object of interest. Aquaporin is a renal protein which mediates the action of vasopressin. In the sphere of stress evidence is emerging on the participation of CRH in brain activity and the possibility to influence autoimmune inflammations and perhaps even AIDS by interference with the CRH-proopiomelanocortin-ACTH-cortisol system.
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PMID:[Endocrinology 1995-1996]. 926 67


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