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)

Posttraumatic diabetes insipidus, acute pancreatitis, and Wernicke's encephalopathy and Korsakoff's psychosis in a 33-year-old white male alcohol abuser resulted in near-fatal cardiovascular collapse. The Wernicke's encephalopathy and Korsakoff's psychosis resulted from drinking massive quantities of beer to satisfy the thirst induced by diabetes insipidus. Although the diabetes insipidus was controlled with vasopressin, and the need for vasopressin resolved two months after diagnosis, the Wernicke-Korsakoff syndrome had not resolved by six months.
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PMID:Korsakoff's psychosis due to massive beer intake provoked by diabetes insipidus. 336 23

Six athletes were examined immediately after collapsing from heat stroke during exercise, and then followed for several weeks. At the time of collapse most of the patients were sweating profusely, their rectal temperatures being more than 42 degrees C. All recovered within a few hours. The renal function was not disturbed more than expected during heavy exercise, serum levels of liver enzymes were, however, increased for several weeks. Electrolyte homeostasis was undisturbed but for a transient hypercalcemia that can not be fully explained. The marked increments in plasma levels of catecholamines, vasopressin and renin were as expected after heavy exercise. We conclude that as heat stroke presents as a continuum of clinical pictures, biochemical evidence of liver cell injury is a sensitive and important parameter for the diagnosis.
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PMID:Heat stroke in endurance exercise. 353 1

The importance of the renal pressure natriuresis and diuresis mechanisms in long-term control of body fluid volumes and arterial pressure has been controversial and difficult to quantitate experimentally. Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. When renal arterial pressure was servo-controlled in these models of hypertension, sodium and water retention continued unabated, causing ascites, pulmonary edema, or even complete circulatory collapse within a few days. Apparently, other mechanisms for volume homeostasis, such as the various natriuretic and diuretic factors that have been postulated, are not sufficiently powerful to maintain fluid balance in the absence of increased renal arterial pressure when renal excretory function is reduced in these forms of hypertension. The intrarenal mechanisms responsible for pressure natriuresis and diuresis are not entirely clear, but they seem to involve small increases in glomerular filtration rate and filtered load as well as reductions in fractional reabsorption in proximal and distal tubules. During chronic disturbances of arterial pressure additional factors, especially changes in AngII and aldosterone formation, act to amplify the effectiveness of the basic renal pressure natriuresis and diuresis mechanisms in regulating arterial pressure and body fluid volumes.
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PMID:Regulation of arterial pressure: role of pressure natriuresis and diuresis. 353 87

A patient bleeding from oesophageal varices in whom injection sclerotherapy failed to control bleeding required peripheral vein vasopressin infusion for a total of five days. Three days after stopping the infusion she collapsed and died. Post mortem examination showed the cause of death to be intestinal infarction resulting from superior mesenteric and portal vein thrombosis. This complication has not previously been described in association with vasopressin infusion into peripheral veins. The duration of each infusion should be minimised and blood volume should be carefully monitored throughout. The condition should be suspected in patients who develop unexplained abdominal pain or collapse following vasopressin treatment.
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PMID:A lethal complication of peripheral vein vasopressin infusion. 387 20

The cardiorespiratory, sympathetic and biochemical effects of T-2 toxin were examined in conscious rats and guinea pigs. The pithed rat preparation was also used to evaluate possible direct effects of T-2 on the heart and vasculature. Injection of T-2 (0.5-2.0 mg/kg i.v.) into conscious rats produced prolonged (6-8 hr) hypertension and tachycardia, followed by hypotension. Total peripheral resistance was increased and cardiac output decreased. In guinea pigs, a steady decrease in pressure and rate occurred. Intravenous administration of T-2 to pithed rats did not alter blood pressure or heart rate at a time when, in conscious rats, both blood pressure and heart rate were increased. Significant elevations of arterial plasma norepinephrine, epinephrine and dopamine occurred after T-2, with metabolic acidosis, hypocarbia and hyperoxemia in both conscious rats and guinea pigs. In the rat, increase in plasma vasopressin and prostacyclin were elevated, but thromboxane and leukotriene C4-immunoreactivity were not changed. In pithed rats, T-2 did not increase basal or stimulated plasma catecholamines but produced the same changes in blood gases, pH and lactate. The LD50 values for i.v. T-2 in the rat and guinea pig were 0.74 and 1.30 mg/kg, respectively. The data are consistent with the hypothesis that T-2 toxin disrupts cellular aerobic metabolism, resulting in lactic acidosis, sympathoadrenomedullary activation, variable initial circulatory responses and eventual cardiovascular collapse.
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PMID:Cardiorespiratory, sympathetic and biochemical responses to T-2 toxin in the guinea pig and rat. 397 27

A 68 year-old woman, treated 30 years ago by collapse therapy for tuberculosis of the lung, presently developed the syndrome of inappropriate antidiuretic hormone scretion. The investigation revealed only an extensive right fibrothorax. The possible relation between the latter and her present illness is discussed.
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PMID:Inappropriate anti-diuretic hormone (ADH) secretion in a patient with extensive fibrothorax. 741 8

Cardiovascular and hormonal responses to anaphylactic shock were evaluated in anaesthetized pigs sensitized by natural exposure to Ascaris suum as verified by antibodies. In six animals with such antibodies, Ascaris antigen injection produced a plasma histamine increase of 52 (42-196) fold (median and range; P < 0.05), while four pigs without such antibodies served as controls with only insignificant increases in histamine. In the anaphylactic group, two of the animals died during the investigation due to cardiovascular collapse. In the sensitized pigs resting heart rate (HR), 104 (86-118) beats min-1, increased to 204 (164-240) beats min-1 as mean arterial pressure (MAP) decreased from 94 (83-102) to 45 (31-90) mmHg (P < 0.05). In contrast, the non-sensitized pigs maintained the resting HR of 101 (79-113) beats min-1, as MAP decreased to 50 (41-97) mmHg (P < 0.05). In the sensitized group systemic vascular resistance (SVR) fell from 1114 (843-1811) to 990 (588-1173) dyne s-1 cm-5 and then increased to 3617 (2593-4166) dyne s-1 cm-5, while in the control group there was only a reduction to a minimum value of 730 (458-1307) dyne s-1 cm-5 (P < 0.05). Thoracic electrical impedance increased only in the sensitized group [from 28.3 (24.7-31.4) to 29.9 (24.0-31.4)], indicating central volume depletion. Plasma catecholamines increased markedly only in the sensitized pigs, and plasma pancreatic polypeptide, vasopressin, aldosterone and renin responses confirmed to those established during central hypovolaemia. During anaphylaxis, this study demonstrated cardiovascular responses similar to those established during a major blood loss. However, as indicated by plasma catecholamines, sympathetic activity was many times that previously demonstrated during haemorrhage, and sympathoactivation may explain the marked vasoconstriction noted in the sensitized pigs.
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PMID:Cardiovascular and hormonal responses to anaphylactic shock in the pig. 771 95

1. The effects of fetal intravenous treatment with phentolamine or a vasopressinergic V1-receptor antagonist on the fetal cardiovascular responses to acute hypoxaemia in the llama were investigated. 2. Six llama fetuses were surgically prepared between 60 and 70 % of gestation under general halothane anaesthesia with vascular catheters and transit-time ultrasonic flow probes around a carotid artery and a femoral artery. At least 4 days after surgery all fetuses were subjected to a 3 h experiment: 1 h of normoxia, 1 h of hypoxaemia and 1 h of recovery while on slow i.v. infusion with saline. On separate days this experiment was repeated with fetal i.v. treatment with either phentolamine or a V1-receptor antagonist dissolved in saline. 3. During saline infusion all llama fetuses responded to acute hypoxaemia with intense femoral vasoconstriction. Phentolamine during normoxia produced hypotension, tachycardia and vasodilatation in both the carotid and the femoral circulations. During hypoxaemia, fetuses treated with phentolamine did not elicit the pronounced femoral vasoconstriction and all died within 20 min of the onset of hypoxaemia. A V1-receptor antagonist produced a femoral vasodilatation during normoxia but did not affect the fetal cardiovascular responses to acute hypoxaemia. 4. In conclusion, alpha-adrenergic and V1-vasopressinergic mechanisms contribute to a basal vasoconstrictor tone in the femoral circulation in the llama fetus. The enhanced femoral vasoconstriction during acute hypoxaemia in the llama fetus is not mediated by stimulation of V1-vasopressin receptors, but is dependent on alpha-adrenergic receptor stimulation. Such alpha-adrenergic efferent mechanisms are indispensable to fetal survival during hypoxaemia in the llama since their abolition leads to cardiovascular collapse and death.
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PMID:Adrenergic and vasopressinergic contributions to the cardiovascular response to acute hypoxaemia in the llama fetus. 992 92

Vasopressin is a vital homeostatic protein which regulates fluid balance via its antidiuretic effects and vascular tone via its vasoconstrictive effects. Endogenous vasopressin deficiency has been implicated in several disease states resulting in vasodilatory shock. In particular, vasopressin levels are low in patients following cardiac surgery and in those with ventricular dysrhythmias. Several recent studies have demonstrated the effectiveness of exogenous vasopressin in providing haemodynamic support in patients with postcardiopulmonary bypass vasodilatory shock and refractory ventricular fibrillation. This manuscript reviews the pathophysiological and clinical basis for vasopressin replacement in patients with cardiovascular collapse.
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PMID:Vasopressin in cardiovascular patients: therapeutic implications. 1199 29

The pregnant llama (Lama glama) has walked for millions of years through the thin oxygen trail of the Andean altiplano. We hypothesize that a pool of genes has been selected in the llama that express efficient mechanisms to withstand this low-oxygen milieu. The llama fetus responds to acute hypoxia with an intense peripheral vasoconstriction that is not affected by bilateral section of the carotid sinus nerves. Moreover, the increase in fetal plasma concentrations of vasoconstrictor hormones, such as catecholamines, neuropeptide Y, and vasopressin, is much greater in the llama than in the sheep fetus. Furthermore, treatment of fetal llamas with an alpha-adrenergic antagonist abolished the peripheral vasoconstriction and resulted in fetal cardiovascular collapse and death during acute hypoxia, suggesting an indispensable upregulation of alpha-adrenergic mechanisms in this high altitude species. Local endothelial factors such as nitric oxide (NO) also play a key role in the regulation of fetal adrenal blood flow and in the adrenal secretion of catecholamines and cortisol. Interestingly, in contrast to the human or sheep fetus, the llama fetus showed a small increase in brain blood flow during acute hypoxia, with no increase in oxygen extraction across the brain, and thereby a decrease in brain oxygen consumption. These results suggest that the llama fetus responds to acute hypoxia with hypometabolism. How this reduction in metabolism is produced and how the cells are preserved during this condition remain to be elucidated.
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PMID:The fetal llama versus the fetal sheep: different strategies to withstand hypoxia. 1285 51


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