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)

A 37-year-old male patient with a diffuse pleomorphic B-cell-lymphoma, which has been diagnosed two month earlier with the primary site at the pterygopalatine fossa on both sides with infiltration of the clivus and cavernous sinus was referred to our hospital for continuation of the third course of CHOP chemotherapy. At admission he reported about a recent history of painful swallowing and intermittent substernal chest pain. Alleviation of the pain on swallowing and the chest pain was apparently only possible by drinking 10 to 15 l of cold coca cola throughout the day and night, a regimen that resulted in polyuria. Physical examination revealed extensive thrush stomatitis and soor esophagitis. Despite successful treatment with fluconazole, polydipsia continued unabated. The classic osmotic test of dehydration and exogenous vasopressin revealed hypothalamic diabetes insipidus (DI). Basal hormones and stimulated endocrine function tests of the adenohypophysis were found to be normal. MRI-scan revealed lymphoma infiltration of the neurohypophysis. After the third course of CHOP chemotherapy the patient surprisingly recovered completely from his excessive thirst. The present report shows that clinical disorders such as thrush stomatitis can mask diabetes insipidus caused by an early relapsing lymphoma.
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PMID:Diabetes insipidus in a patient with a highly malignant B-cell lymphoma and stomatitis. 1096 68

We investigated whether arginine vasopressin (AVP) has a central influence on the development of gastric mucosal lesions evoked by restraint-cold stress in rats. AVP and vasopressin V1 receptor antagonist were injected intracerebroventricularly (i.c.v.) and the rats were exposed to restraint-cold stress for five hours. After decapitation the stomachs were examined for gastric mucosal lesions which were evaluated according to an ulcer score. Three different doses of AVP and V1 receptor antagonist were administered in order to investigate the effects of exogenous and endogenous AVP on stress-induced gastric mucosal lesions. The intensity of gastric mucosal lesions was reduced when exogenous AVP was injected intracerebroventricularly. On the other hand, vasopressin V1 receptor antagonist, which was administered by the same route, augmented gastric mucosal lesions. Our findings indicate that AVP, injected centrally, plays a role in preventing the formation of gastric mucosal lesions induced by stress via a central V1 receptor.
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PMID:Role of intracerebroventricular vasopressin in the development of stress-induced gastric lesions in rats. 1078 10

The gaseous neuromodulator carbon monoxide has been shown to reduce the stimulated release of stress neuropeptides, such as vasopressin and oxytocin, from the rat hypothalamus in vitro, while evidence concerning corticotropin-releasing hormone is controversial. In vivo studies have been conducted in the rat, inhibiting heme oxygenase activity--and hence carbon monoxide biosynthesis--in the central nervous system by means of specific heme oxygenase blockers; these studies showed that basal heme oxygenase activity tends to oppose exaggerated increases in vasopressin secretion following immune-inflammatory challenges, whereas it favors the normal rise in circulating ACTH which follows footshock. Another gas normally produced in mammalian brains under basal conditions, hydrogen sulfide, also appears to play a role in the control of the hypothalamo-pituitary-adrenal axis. Indeed, increases in hydrogen sulfide levels within the hypothalamus, either obtained with hydrogen sulfide-enriched media or by the addition of the hydrogen sulfide precursor S-adenosyl-methionine, are associated with the inhibition of the stimulated release of corticotropin-releasing hormone from rat hypothalamic explants. Parellel in vivo experiments in the rat under resting conditions and after stress-induced adrenocortical activation show that S-adenosyl-methionine significantly reduces the rise in serum corticosterone levels caused by 1-h exposure to cold. These results demonstrate the pathophysiological importance of both carbon monoxide and hydrogen sulfide in the regulation of neuroendocrine function.
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PMID:Gaseous neuromodulators in the control of neuroendocrine stress axis. 1126 92

The effects of cold-restraint stress, repeated over 3 days, and treatment of rats with vasoactive intestinal peptide (VIP) on the contractile responses of isolated aorta to vasoconstrictors, and on aortic adventitial mast cells were investigated. Stress significantly reduced the contractile response of rat aorta smooth muscle to norepinephrine (NE), angiotensin II (Ang II) and vasopressin (VP). Decreased sensitivity to NE, Ang II and VP may result from decreased receptor density, and affinity or reduced effector efficacy. Stress induced degranulation, decreased the number and changed the granular content of mast cells; all degranulated mast cells were stained with alcian blue, and the percentage of safranin staining cells was decreased. Given prior to stress, VIP reversed the reduced contractile responses and sensitivity of aorta to NE and Ang II but had no effect on VP subsensitivity. VIP also inhibited stress-induced degranulation of mast cells, and after VIP only alcian blue-stained mast cells were seen. When VIP was given to non-stressed rats, the contractile response of the aorta to NE, but not Ang II or VP, was increased compared with control. Mast cell count was decreased in the adventitia of non-stressed VIP treated rats. The results indicate that stress decreases the heparin content of mast cells and VIP has an additive effect. In conclusion, VIP modulates both stress-induced mast cell activity and reduced sensitivity of aorta smooth muscle to NE and Ang II. It can be suggested that VIP may moderate some effects of stress on vascular pathophysiology.
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PMID:The effect of stress and in vivo vasoactive intestinal peptide (VIP) treatment on the response of isolated rat aorta to norepinephrine, angiotensin II and vasopressin, and adventitial mast cells. 1134 95

Recent studies, which have shown an increase of plasma vasopressin (VP) in experimental motion sickness and the efficacy of VP antagonists for motion sickness, suggest an important role of VP in the development of vestibulo-autonomic responses. We have recently found evidence of the co-existence of vasopressinergic neurons with the stress-sensitive chemokinergic neuronal system in the hypothalamo-pituitary pathway in rats, which uses cytokine-induced neutrophil chemoattractant (CINC) as an effector molecule. In this study, to elucidate possible roles of VP and CINC in the vestibulo-autonomic responses, we simultaneously measured plasma VP and CINC concentrations after electrical or caloric vestibular stimulation in urethane-anesthetized rats. Electrical vestibular stimulation with more than 200 microA increased the plasma levels of VP in a current intensity-dependent manner, and stimulation with 500 microA increased the plasma VP levels to 350% of the normal control group, which received no stimulation. Caloric vestibular stimulation with cold water increased the plasma VP levels to 262% of the control group, which received caloric stimulation with water at 37 degrees C, and stimulation with warm water tended to increase the plasma VP levels. Plasma CINC levels were neither affected by electrical nor caloric vestibular stimulation. These findings indicate that vestibular stimulation increased plasma levels of VP but not CINC, and this vestibular-induced activation of VP neurons may be involved in a mechanism of vestibulo-autonomic responses.
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PMID:Vestibular modulation of plasma vasopressin levels in rats. 1157 10

Infant rats respond to cold exposure with increased heat production by brown adipose tissue (BAT). BAT thermogenesis increases steadily with increasing cold exposure, but a point occurs at which thermogenesis can increase no further, resulting in cold-induced bradycardia. Previous work has shown that mean arterial pressure (MAP) is maintained even when cardiac rate decreases as much as 50% from baseline values. We examined the neural and hormonal contributions to peripheral resistance during cold exposure after pups were injected subcutaneously with vehicle, an alpha1-adrenoceptor antagonist (prazosin; 0.5 mg/kg), an ANG II receptor antagonist (losartan; 1 mg/kg), a vasopressin receptor antagonist (Manning compound; 0.5 mg/kg), or simultaneous administration of all three antagonists (triple block). Interscapular temperature, oxygen consumption, cardiac rate, and arterial pressure were monitored as air temperature was sequentially decreased from thermoneutral (i.e., 35 degrees C) to 29, 23, and 17 degrees C. Only pups in the triple block condition exhibited significant decreases in MAP with cooling, even though all pups exhibited substantial decreases in cardiac rate. A followup study suggested that blockade of all three systems was more effective than blockade of any two systems. Finally, at 17 degrees C, ultrasonic vocalizations were accompanied by significant increases in MAP, replicating a previous finding and supporting the hypothesis that the vocalization is the acoustic by-product of the abdominal compression reaction, a maneuver that helps to maintain venous return during cardiovascular challenge.
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PMID:Neural and hormonal control of arterial pressure during cold exposure in unanesthetized week-old rats. 1164 Nov 23

Salt loading decreases body core temperature (T(core)) at neutral ambient temperature (26 degrees C) and increases heat-escape/cold-seeking behaviour in desalivated rats. In this study, we tested the hypothesis that brain angiotensin II (AII) and arginine vasopressin (AVP) are associated with these responses. Surgically desalivated rats (n = 28) were administered an injection (S.C., 10 ml kg(-1)) of either normal saline (154 mM, NS) or hypertonic saline (2500 mM, HS) following an intracerebroventricular injection (10 microl kg(-1)) of an AII AT(1)-receptor antagonist (candesartan, 5 microg microl(-1)), an AVP V(1)-receptor antagonist ((beta-mercapto-beta, beta-cyclopenta-methylene propionyl(1), O-Me-Tyr(2), Arg(8))-vasopressin, 0.5 microg microl(-1)), or normal saline (154 mM). Each rat was placed in a behaviour box, first at 26 degrees C for 1 h to allow the measurement of baseline T(core) and movement. The ambient temperature was then elevated to 40 degrees C for the next 2 h, during which time the rat was able to trigger a 0 degrees C air reward for 30 s by moving into a specific area of the box (operant behaviour). The S.C. HS significantly decreased baseline T(core) at 26 degrees C (36.5 +/- 0.1 degrees C) and increased counts of operant behaviour at 40 degrees C (57 +/- 3) compared with results obtained following S.C. NS injection (37.4 +/- 0.1 degrees C and 42 +/- 1, respectively). These responses to s.c. HS were inhibited by the intracerebroventricular injection of AT(1) (37.3 +/- 0.1 degrees C and 43 +/- 2, respectively; P < 0.05) and V(1) antagonists (37.2 +/- 0.2 degrees C and 42 +/- 2, respectively; P < 0.05), although administration of both antagonists with S.C. NS had no effect. These results suggest that brain AII and AVP are involved in the decrease in T(core) observed at neutral ambient temperature and the increase in heat-escape/cold-seeking behaviour in response to osmotic stimulation, via the central AT(1) and V(1) receptors, respectively
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PMID:Systemic salt loading decreases body temperature and increases heat-escape/cold-seeking behaviour via the central AT1 and V1 receptors in rats. 1243 68

The aim of this study was to assess our hypothesis that the release of antidiuretic hormone (ADH), the renal concentrating response to ADH, or both is decreased by prolonged cold exposure. Six groups (n = 6/group) of rats were used. Three groups were exposed to cold (5 degrees C), whilethe remaining three groups were kept at room temperature (25 degrees C). It was found that urine osmolality decreased significantly and serum osmolality increased significantly during cold exposure. The ratio of water/food intake was not affected by prolonged cold exposure. However, prolonged cold exposure increased the ratio of urine output/food intake in the cold-exposed rats, indicating that more urine flow is required by the cold-exposed rats to excrete the osmotic substance at a given food intake. The difference between water intake and urine output decreased significantly in the cold-exposed rats. Thus, prolonged cold exposure increases water loss from excretion. Renal concentrating responses to 24-h dehydration and Pitressin were decreased significantly in the cold-exposed rats. Plasma ADH levels remained unchanged, but renal ADH receptor (V2 receptor) mRNA was decreased significantly in the cold-exposed rats. The results strongly support the conclusion that cold exposure increases excretive water loss, and this may be due to suppression of renal V2 receptors rather than inhibition of ADH release.
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PMID:Renal responses to chronic cold exposure. 1266 54

The aim of the present study was to examine whether minimizing plasma volume loss due to cold-induced diuresis can increase the survival time of rats maintained in long-term stable hypothermia (~24 h at a body temperature of 19 degrees C). Infusion of desmopressin (0.5-2.0 microg), a potent antidiuretic agent, during the cooling period enhanced survival over saline controls in a dose-related manner. The enhanced survival was accompanied by a significant delay in the expected increase of hematocrit and decrease of plasma volume as compared with those seen in saline controls. In contrast, treating the rats with the same dose range of another vasopressin analog, [beta-mercapto-beta,beta-cyclopentamethyl enepropionyl]-vasopressin, which has no antidiuretic action, failed to enhance survival over saline control. Further, treating the rats with the optimal dose of desmopressin (1 microg) at the later stage of hypothermia failed to elicit any beneficial effect. Our results indicate that by using desmopressin early during the cooling phase of the hypothermia, plasma volume and rheological parameters important for sustaining microcirculation can be better maintained than those seen in saline controls. These improvements may have contributed to the observed longer survival time in hypothermia.
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PMID:Effects of desmopressin on prolonging survival in stable hypothermia in rats. 1461 29

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
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PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84


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