UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intact adult male rats fed an alcohol [ethanol (EtOH)] diet for 10 days show blunted adrenocorticotropic hormone (ACTH) release in response to immune signals such as the cytokine interleukin-1 beta (IL-1 beta) and endotoxin [lipopolysaccharide (LPS)], as well as to physical stress (mild electroshocks). The mechanisms responsible for this effect remain poorly understood, but we have recently reported that decreased pituitary responsiveness to vasopressin (VP) might play a role. In naive rats, nitric oxide (NO) exerts a restraining influence on the response of the hypothalamic-pituitary (H-P) axis to cytokines and VP. The ability of long-term EtOH treatment to increase glutamate receptors, and thus NO formation, prompted us to test the hypothesis that abnormally high NO concentrations might modulate the influence of the drug. Blockade of the activity of NO synthase (NOS), the enzyme responsible for NO formation, with the arginine derivative L-N omega nitro-L-arginine-methylester (L-NAME), augmented the ACTH response to IL-1 beta or LPS in both control (C) and EtOH-fed (E) rats. Indeed, after L-NAME treatment, ACTH concentrations were statistically comparable in C and E animals injected with endotoxin or a large dose of IL-1 beta. VP-induced ACTH secretion also became comparable in both experimental groups after blockade of NOS activity. In contrast, the decreased response of the H-P axis of E animals to shocks was only slightly ameliorated, compared with that of C rats. It is therefore possible that changes in the NOergic tone induced by alcohol play a role in the decreased response of the H-P axis to cytokines, possibly in part by altering the stimulatory action of VP on the corticotrophs. On the other hand, in E rats NO seems to exert only a minimal influence on the central nervous system circuits activated by shocks.
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PMID:Adult male rats exposed to an alcohol diet exhibit a blunted adrenocorticotropic hormone response to immune or physical stress: possible role of nitric oxide. 874 13

Endogenous neuropeptides such as vasopressin, adrenocorticotropin and opioids have significant effects on learning and memory. However, because of the complexity of behaviour, that is defined as 'learning' and 'memory' and, because of the limitation of current knowledge, it has been difficult to interpret these behavioural data, especially via neural mechanisms. The application of modern experimental techniques including molecular biology such as cloning and electrophysiology, such as patch-clamp, has had a significant impact upon the concepts about drugs, including neuropeptides action sites. This allows us to try to interpret some behavioural consequences influenced by neuropeptides. The data on effects of some neuropeptides on behaviours and their possible mechanisms are reviewed. Whatever the mechanisms, vasopressin, adrenocorticotropic hormone and endogenous opioids seem to have important effects upon learning and memory and these open up the possibility that drugs enhance cognitive functions or treat dementia via alteration of functions of neuropeptides. Some criteria are proposed for evaluating the validity of behavioural tests for neuropeptides.
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PMID:The role of neuropeptides in learning and memory: possible mechanisms. 877 Oct 46

A comparative study of the effects of intravenously administered corticotropin releasing factor (i.e. exogenous CRF), in the absence or presence of simultaneous opioid receptor blockade, versus stress (i.e. endogenous CRF) on plasma adrenocorticotropic hormone (ACTH), cortisol and vasopressin (AVP) was carried out in ten healthy men (mean age 35.6 +/- 9.5 years) using an intra-individual repeat setting. Three different stimuli were applied blindly and in random order, one per day, in a 3-day experimental block: (1) human (h) CRF; (2) hCRF/naloxone; and (3) a combined multifaceted 5-min stress test. A second block, following the same protocol, was carried out 12 weeks later. Each experimental day lasted from 0700 to 1500 hours, with subjects remaining supine throughout. ACTH and cortisol levels each responded with significant peaks to all three stimulating conditions in both blocks while AVP levels remained unaffected by any of these stimuli. Unexpectedly, in five of the ten subjects significantly elevated AVP basal concentrations were measured throughout the first block. This phenomenon appeared to be age-related, being observed in younger men only (29.6 +/- 5.2 vs 41.6 +/- 9.2 years; p = 0.03) and was not paralleled by changes in plasma osmolality or blood pressure. In the second block, AVP levels were low and no longer different between younger and older subjects. ACTH and cortisol curves did not differ among subgroups nor between blocks. In conclusion, plasma AVP, in contrast to ACTH, is not acutely influenced by either endogenous or exogenous CRF. However, anticipation of novelty seems to be a human-specific, stress-related stimulus for a sustained elevation of plasma AVP in young men. This novelty-related continuous elevation of AVP levels reported here neither affected basal plasma ACTH nor acted synergistically with exogenous hCRF to increase circulating ACTH.
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PMID:A novelty-related sustained elevation of vasopressin plasma levels in young men is not associated with an enhanced response of adrenocorticotropic hormone (ACTH) to human corticotropin releasing factor (hCRF). 901 Sep 61

ANAESTHETICS, ENDOCRINE SYSTEM, AND STRESS: The effects of anaesthetics on the nervous system are invariably associated with endocrine reactions, which are of great importance for the general characterization of anaesthetics or anaesthetic regimens. In this context, the endocrine stress response is mainly represented by adrenaline (A), noradrenaline (NA), antidiuretic hormone/vasopressin (ADH), adrenocorticotropic hormone (ACTH), and cortisol. PHARMACOLOGICAL PROFILE AND ANAESTHETIC ACTION OF KETAMINE: The pharmacological profile of ketamine is characterized by the term "dissociative anaesthesia." At the present time, the anaesthetic action of ketamine cannot be explained by a single mechanism. Its overall action might be due to different central and peripheral factors, and stereospecific effects are obvious. ENDOCRINE RESPONSES TO RACEMIC KETAMINE AND S(+)-KETAMINE: In contrast to stereospecific differences in the anaesthetic action of racemic ketamine and S-(+)-ketamine, the endocrine reactions to the S-(+) isomer and the racemic mixture are very similar. When S(+)-ketamine is used as the sole anaesthetic, significant activation of the sympathoadrenergic system with increases in plasma levels of A and NA can be observed. This effect is mitigated by midazolam. In combination with propofol, sympathoadrenergic responsiveness is preserved without overwhelming effects. In contrast to monoanaesthesia with S(+)-ketamine, during combination with midazolam and propofol significant increases in plasma ADH levels are observed, which might be due to suppressed sympathoadrenergic reactivity. In addition, surgical stress activates the pituitary-adrenocortical system with increases in ACTH and cortisol. Effects of midazolam and propofol on this effect are similar. SYNOPSIS AND CLINICAL ASPECTS: S-(+)-ketamine as a monoanaesthetic has significant sympathomimetic properties, which are beneficial during induction of patients in shock and patients with asthma. The combination of S-(+)-ketamine and midazolam has weaker sympathomimetic and general endocrine-stimulating properties, and can be used for analgosedation in patients with cardiovascular instability and exogenous catecholamine requirements. In combination with propofol, the sympathomimetic and general endocrine-stimulating effects of S-(+)-ketamine are less pronounced because of contrasting properties of both drugs. This combination might be useful in patients with endocrine deficits and for analgosedation, when rapid recovery is necessary and negative circulatory effects should be avoided.
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PMID:[Endocrine reactions following S-(+)-ketamine]. 916 76

The adipose tissue-derived hormone leptin regulates body weight homeostasis by decreasing food intake and increasing energy expenditure. The weight-reducing action of leptin is thought to be mediated primarily by signal transduction through the leptin receptor (LR) in the hypothalamus. We have used immunohistochemistry to localize LR-immunoreactive (LR-IR) cells in the rat brain using an antiserum against a portion of the intracellular domain of LR that is common to all LR isoforms. The antiserum recognized the short and long isoforms of LR in transfected hematopoietic BaF3 cells. To examine the chemical nature of target cells for leptin, direct double-labeling immunofluorescence histochemistry was applied. The results show extensive distribution of LR-like immunoreactivity (LR-LI) in the brain with positively stained cells present, e.g., in the choroid plexus, cerebral cortex, hippocampus, thalamus, and hypothalamus. In the hypothalamus, strongly LR-IR neurons were present in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), periventricular nucleus, arcuate nucleus, and lateral hypothalamus. Weaker LR-IR neurons were also demonstrated in the lateral and medial preoptic nuclei, suprachiasmatic nucleus, ventromedial and dorsomedial nuclei, and tuberomammillary nucleus. Confocal laser scanning microscopy showed LR-LI in the periphery of individual cells. In magnocellular neurons of the SON and PVN, LR-LI was demonstrated in vasopressin- and oxytocin-containing neurons. In parvocellular neurons of the PVN, LR-LI was demonstrated in many corticotropin-releasing hormone-containing neurons. LR-IR neurons were mainly seen in the ventromedial aspect of the arcuate nucleus, where LR-LI co-localized with neuropeptide Y. In the ventrolateral part of the arcuate nucleus, LR-LI was present in many large adrenocorticotropic hormone-IR proopiomelanocortin-containing neurons and in a few galanin-, neurotensin-, and growth hormone-releasing hormone-containing neurons. In the dorsomedial arcuate nucleus, few tyrosine hydroxylase (dopamine)-containing neurons were seen to have LR-LI. Melanin-concentrating hormone-containing neurons in the lateral hypothalamus had LR-LI. Based on the immunohistochemical results, possible interactions of leptin with brain mechanisms are discussed.
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PMID:Leptin receptor immunoreactivity in chemically defined target neurons of the hypothalamus. 941 31

The cardiovascular and humoral responses to sustained muscle metaboreflex activation were examined in eight male volunteers while they performed two 24-min exercise protocols. Each of these consisted of six 1-min bouts of isometric handgrip exercise (the left and right hands being used alternately) at 50% of maximal voluntary contraction; after each bout, there was either 3-min postexercise occlusion (occlusion protocol) or 3-min rest (control protocol). In the occlusion protocol, mean arterial blood pressure was approximately 25 mmHg higher than during the control protocol, indicating that the muscle metaboreflex was activated during occlusion. During the control protocol, plasma renin activity, plasma vasopressin, and adrenocorticotropic hormone values were not significantly different from the values at rest. During the occlusion protocol, however, plasma renin activity, plasma vasopressin, and adrenocorticotropic hormone were all significantly increased at 25 min. These data demonstrate that, in humans, the sustained activation of the muscle metaboreflex causes the secretion of several hormones originating from different regions.
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PMID:Cardiovascular and humoral responses to sustained muscle metaboreflex activation in humans. 945 25

Plasma cortisol increases in fetuses at term and is important for overall development. This study was designed to determine whether cortisol increases synchronously in twin fetal sheep and whether differences between twins contribute to the respective timing. Catheters were surgically implanted in fetal arteries in twins, the amniotic sac, and a maternal artery and vein. Blood was drawn daily until labor was imminent or the twins were delivered. Fetal pituitaries and adrenals were removed for in vitro measurements. Analyses included blood gases and cortisol (daily) and plasma cortisol, adrenocorticotropic hormone (ACTH), and estrogens (at completion). Twins were assigned retrospectively to group A or B, depending on which cortisol was first elevated (group A) above baseline. Group A fetuses consistently had higher cortisol until term. All group A fetuses also first had elevated ACTH. In four of four sets of twins of both sexes, the male was in group A. There were no differences between fetuses in plasma estrogens or pituitary ACTH response to stimulation, but adrenal cells from group A fetuses were more responsive. These data suggest that adrenal activity is increased in one twin consistently, with the difference being attributable to the responsiveness of adrenal cells to ACTH rather than pituitary responsiveness to either corticotropin-releasing hormone or vasopressin. Difference between sexes may also be involved.
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PMID:Development of the pituitary adrenal axis in fetal sheep twins. 945 91

A 44-year-old woman with Marie-Bamberger's syndrome and diabetes insipidus had a lung tumour with mediastinal metastases, but no signs of metastases to the hypothalamus or pituitary gland. A week after removal of the tumour, the joint pain, polyuria and polydipsia disappeared. The tumour was diagnosed histopathologically as a moderately differentiated adenocarcinoma with focal neuroendocrine cell differentiation and dispersed cells reacting with antisera against neurone-specific enolase, S-100 protein, neuropeptide Y, follicle-stimulating hormone, substance P, vasoactive polypeptide (VIP), adrenocorticotropic hormone and pancreatic polypeptide (PP) as well as to one of three tested antisera raised against antidiuretic hormone (ADH). It was suggested that Marie-Bamberger's syndrome might be caused by one of these immunoreactive substances or by a substance that shares an amino acid sequence with one of these neuroendocrine peptides. It was also suggested that the tumour might produce an ADH-like substance which might have an ADH-antagonist effect.
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PMID:Recovery from Marie-Bamberger's syndrome and diabetes insipidus after removal of a lung adenocarcinoma with neuroendocrine features. 956 47

In the present study, we examined denervation-induced changes in the sensitivity of hypothalamic postsynaptic serotonin1A (5-HT1A) receptor function with respect to changes in the dose-dependent elevation in plasma hormones [adrenocorticotropic hormone (ACTH), corticosterone, prolactin, oxytocin, prolactin, renin and vasopressin] by the 5-HT1A agonist 8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT). Rats received intracerebroventricular (i.c.v.) injections of the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) or vehicle (0.1% ascorbate in saline) 3 weeks before challenge with increasing doses of 8-OH-DPAT (0, 10, 50 or 200 micrograms/kg s.c.). The effectiveness of 5,7-DHT-induced destruction of serotonergic neurons was confirmed by a 93% reduction in [3H]paroxetine-labeled 5-HT uptake sites in the hypothalamus. No changes in basal levels of ACTH, corticosterone, oxytocin, prolactin, renin and vasopressin were observed in rats that received i.c.v. 5,7-DHT injections. The dose-response curves for 8-OH-DPAT-induced elevations of plasma corticosterone and prolactin levels were shifted to the left in rats treated with 5,7-DHT, whereas no significant difference in the ACTH dose-response curve was observed between rats treated with vehicle and rats treated with 5,7-DHT. In contrast, the maximal oxytocin response to 8-OH-DPAT was attenuated in rats treated with 5,7-DHT. A 5,7-DHT-induced decline in the synthesis of oxytocin could explain this phenomenon. Although 8-OH-DPAT did not increase plasma levels of renin or vasopressin in rats treated with vehicle, 8-OH-DPAT produced an elevation (75%) in plasma renin concentration but not in vasopressin levels in rats that received i.c.v. injections of 5,7-DHT. No change was observed in [3H]8-OH-DPAT labeled 5-HT1A receptors in the hypothalamus. In summary, denervation of hypothalamic serotonergic nerve terminals produces supersensitivity of some neuroendocrine responses to 8-OH-DPAT independent of changes in the density of hypothalamic 5-HT1A receptors.
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PMID:Alterations in 8-hydroxy-2-(dipropylamino)tetralin-induced neuroendocrine responses after 5,7-dihydroxytryptamine-induced denervation of serotonergic neurons. 965 67

The pituitary-adrenal secretory response to acute and chronic stress, suppressibility of adrenocortical secretions by exogenous glucocorticoids, and hypothalamic content and in vitro release of the two major peptidergic activators of the hypothalamo-pituitary-adrenal (HPA) axis, corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP), were examined in rats receiving daily melatonin (MEL) injections coincident with the circadian increment of endogenous pineal and adrenocortical secretory activity. After 7 days of MEL administration, the rats displayed a significant attenuation of the adrenocortical secretory response to acute and chronic stress. Chronic MEL treatment also prevented the decline in adrenocorticotropic hormone (ACTH) release resulting from chronic stress exposure. Hypothalamic CRH content was significantly lower in rats receiving MEL treatment, while AVP remained largely unaltered; however, MEL administration counteracted the chronic stress-induced decrease in hypothalamic AVP content and in vitro release. When exposed to dexamethasone in vitro, hypothalamic explants from MEL-treated rats responded with a stronger suppression of CRH and AVP release than those originating from vehicle-injected animals. These observations indicate that MEL attenuates the adrenocortical response to stress and influences the biosynthesis, release and glucocorticoid responsiveness of hypothalamic ACTH secretagogues.
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PMID:Chronic melatonin treatment and the hypothalamo-pituitary-adrenal axis in the rat: attenuation of the secretory response to stress and effects on hypothalamic neuropeptide content and release. 967 11

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