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)

Vasopressin is shown to be a potent mitogen for Swiss 3T3 cells. The hormone (1--10 ng/ml) causes a striking shift of the dose--response curve for the effect of serum on thymidine incorporation by cultures of 3T3 cells arrested in the G1/G0 phase of the cell cycle. In the absence of added serum, the effect of vasopressin on DNA synthesis is greatly potentiated by insulin, epidermal growth factor, and a factor isolated from medium conditioned by simian virus 40-infected baby hamster kidney cells. The mitogenic effect of vasopressin is dependent on time and hormone concentration. In the presence of insulin, the half-maximal effect elicited by the peptide is obtained at 0.6 ng/ml. [Arg]Vasopressin and [Lys]vasopressin are equally potent. The vasopressins are 10(3)-fold more potent than oxytocin. In the presence of a low (2.5%) concentration of serum, vasopressins stimulate cell proliferation.
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PMID:Vasopressin stimulation of mouse 3T3 cell growth. 31 1

For the initial control of haemorrhage from oesophageal varices, two methods of vasopressin administration have been compared--the conventional bolus of 20 units and a low dose infusion of 0.4 units per minute. Twenty patients bleeding from oesophageal varices, confirmed by endoscopy, were allocated into either treatment group (10 in each). Vasopressin infusion stopped bleeding in 86 per cent of the episodes in contrast to 12.5 per cent (P less than 0.01) with bolus doses. Balloon tamponade with a Sengstaken-Blakemore tube was used to control bleeding in only 2 episodes in patients on infusion and in 10 episodes in patients on bolus doses of vasopressin (P less than 0.05). Our study confirms that low dose vasopressin infusion in more effective in controlling bleeding from oesophageal varices than conventional bolus doses.
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PMID:Emergency treatment of variceal haemorrhage. 31 46

Generally, the CRF-like activity of vasopressin is studied in experiments involving adrenalectomy and corticosteroid replacement. In order to avoid this complex type of stress, male and female (diestrus, estrus) rats were exposed to 5 min to immobilization stress and sacrificed 5, 15, and 30 min thereafter. After a survival period of 5 min the vasopressin-synthesizing part of the paraventricular nucleus exhibited an increased activity. Vasopressin-reactive axons in the pericapillary layer of the median eminence and among the solid cell clusters of the pars tuberalis became more conspicuous and increased in number. In this group of experimentally treated animals the prechiasmatic division of the supraoptic nucleus did not show any changes in immunoreactivity. The same holds true for the neurohypophyses in all experimental groups. In animals with increased survival times the supraoptic nucleus exhibited a slightly increased activity, whereas the staining intensity of the paraventricular nucleus decreases gradually. From these results it can be concluded that the paraventricular nucleus is involved in the first phase of the stress response. The problem of vasopressin or a very similar peptide synthesized in this nucleus and exerting a CRF-releasing function is discussed.
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PMID:Altered pattern of vasopressin distribution in the hypothalamus of rats subjected to immobilization stress. An immunohistochemical study. 35 Apr 10

An electron microscopic study was made of mouse pituitaries immunocytochemically stained with anti-lysine vasopressin (LVP) as the primary antiserum in the unlabeled antibody peroxidase-anti-peroxidase procedure. Vasopressin (VP) was identified in the neurosecretory granules of the neural lobe which stained with peroxidase anti-peroxidase molecules. Electron density was induced in secretory granules of the pars intermedia (PI), both in the melanocyte stimulated hormone and ACTH cell types, probably indicating VP molecules attached to binding (receptor) sites. Omission of anti-LVP abolished staining both in the neural lobe and the PL Anti-LVP absorbed with antigen, by admixing with LVP, abolished staining in the neural lobe but not in the PI; according to optical density measurements the PI showed a +/- 22% staining increase over controls. Staining intensity in the PI probably reflects occupancy of binding (receptor) sites for VP. Exposure of PI granules to LVP before the usual staining sequence resulted in +/- 48% increased staining. In water-deprived mice with high endogenous VP titers, staining was +/- 33% and +/- 40% more intense than in normal mice. Solid phase absorbed and eluted antibodies to LVP provided additional proof that staining in both neural lobe and PI could be attributed to anti-LVP. Results indicate that binding or receptor sites for VP are located on secretory granules in the PL Possible physiological significance is discussed.
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PMID:Immunocytochemical evidence for vasopressin receptors. 35 43

Toad bladder epithelial cells were isolated under mild conditions in a calcium-free medium; they were found to exclude trypan blue, to consume oxygen, and to respond to vasopressin with an increased rate of oxygen consumption. Since isolated toad bladder epithelial cells are mostly spherical in shape, the cell diameter can be accurately measured with an ocular micrometer of an inverted microscope. Epithelial cells swelled by 29+/-3% in the presence of KCN. This cyanide-induced swelling of cells was prevented by amiloride or, alternatively, by replacing NaCl by equiosmotic amounts of mannitol in the Ringer's fluid. Cells incubated in the presence of vasopressin swelled by 10+/-2%. Vasopressin and KCN acted synergistically in enhancing cell volume. Ouabain caused cells to swell by 9+/-2%, and this effect was not additive to the swelling seen with vasopressin. These observations are in accord with the theory of Leaf and his associates, that the predominant effect of vasopressin is to enhance sodium entry into the transporting epithelial cells of the toad urinary bladder.
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PMID:Action of vasopressin, ouabain, and cyanide on the volume of isolated toad bladder epithelial cells. 40 62

The effects of vasopressin on blood flow in the superior mesenteric artery and on mean arterial pressure and portal venous pressure were measured in 7 rhesus monkeys. Vasopressin was injected, as either a bolus, or infused both intravenously and intraarterially to assess the influence of the route of administration upon hemodynamic responses. Dose-dependent decreases in superior mesenteric arterial flow were observed during both intraarterial and intravenous injections of vasopressin. No statistically significant differences between the two routes of administration, the decrease in flow, and changes in pressure were observed. Based upon these observations, one might anticipate that intravenously administered vasopressin will be as effective as intraarterially administered vasopressin in reducing mesenteric blood flow, and thus portal venous pressure, in man.
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PMID:Primate mesenteric blood flow. Effects of vasopressin and its route of delivery. 41 90

Vasopressin-induced glucose release from the perfused livers of fed rats is diminished in the presence of insulin or following adrenal ablation. The reduced rate of glucose release following vasopressin treatment in the perfused livers of adrenalectomized rats was restored towards the control value by cortisol treatment in vivo. Vasopressin did not influence the total rate of fatty acid synthesis in the livers of fed rats perfused with medium containing glucose and two concentrations of lactate. The contribution of these precursors to hepatic fatty acid synthesis and CO2 production was similarly uninfluenced by vasopressin. Vasopressin casued a transient increase in the release of K+ by the perfused liver which was observed within 2 min of hormone administration. These results are discussed in relation to the possible mode of action of vasopressin in the liver.
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PMID:The control by vasopressin of carbohydrate and lipid metabolism in the perfused rat liver. 42 22

Sections of the hypothalamus, median eminence and pituitary from fetal and neonatal rats were examined with the immunoperoxidase staining technique and light microscopy. Purified antisera raised against vasopressin and oxytocin, and antisera cross-reactive with rat neurophysin were used to localize these antigens in the hypothalamo-neurohypophysial system (HNS). Neurophysin was detected throughout the HNS of the 18-day fetal rat. Vasopressin was present in the hypothalamus and pituitary of the 19-day fetus, and in the median eminence of the 4-day neonate. Oxytocin was not detected in the pituitary until 1--2 days after birth, in the hypothalamus after 4 days, and in the median eminence after 8 days. During the first days after birth the supraoptic nucleus was more mature than the paraventricular nucleus. The HNS did not approach maturity until at least 7 days after birth. The relative maturity of the supraoptic nucleus compared with the paraventricular nucleus, and the detection of vasopressin before oxytocin are evidence for the one-neuron-one-hormone theory. The data do not exclude the possibility that the fetal hypothalamo-neurohypophysial system, and perhaps the fetal hormone, vasotocin, affect the initiation and course of parturition.
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PMID:Maturation of the hypothalamo-neurohypophysial system. I. Localization of neurophysin, oxytocin and vasopressin in the hypothalamus and neural lobe of the developing rat brain. 43 49

Vasopressin has been used with increasing frequency to control gastrointestinal bleeding, the beneficial effect being attributed to marked splanchnic vasoconstriction. Because vasopressin may result in impaired cardiac function and because other potent vasoconstrictive substances have been shown to increase the pulmonary shunt and decrease arterial oxygenation, this study was undertaken to determind the effect of vasopressin on oxygen availability. Ten healthy anesthetized mechanically ventilated dogs received a five hour intravenous vasopressin infusion, 0.005 U/kg/min. The heart rate decreased moderately and briefly. The mean systemic arterial pressure increased and then decreased, both minimally. The pulmonary shunt and the arterial oxygen content decreased slightly. The total systemic resistance increased and the stroke volume decreased, both substantially. The pulmonary artery wedge pressure gradually increased. The oxygen availability decreased markedly. This study demonstrated that a vasopressin infusion causes a marked decrease in oxygen availability due primarily to a decreased stroke volume and, to a lesser extent during the first hour, to a decreased heart rate. The pulmonary shunt did not increase. Increased systemic resistance followed by a gradual increase in the pulmonary wedge pressure suggests that the decreased stroke volume resulted, at least in part, from an increased afterload and left ventricular failure. It is suggested that until the effect of vasopressin on the cardiopulmonary systems and hence oxygen availability is fully studied in critically ill patients, that it be used with caution and with appropriate hemodynamic monitoring.
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PMID:The effect of vasopressin on oxygen availability. 44 98

We describe a patient with hypothalamic diabetes insipidus who after 20 years became refractory to the effect of commercial vasopressin injection. Vasopressin antibodies were measured using a sensitive hemagglutination technique. Resistance was associated with a high titer of antibodies that disappeared once vasopressin therapy was withdrawn and the diabetes insipidus was controlled with chlorpropamide. Antibodies were also measured in four additional patients with diabetes insipidus while they were or were not receiving vasopressin. A patient who had received the drug for only two years already had a substantial titer of antibodies to vasopressin, but in this case the response to the hormone was not impaired.
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PMID:Clinical resistance to vasopressin. Detection of antibody by hemagglutination. 44 72


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