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)

Changes in rheological properties of the blood were produced by intravenous injection of a high-molecular weight dextran and lysin-vasopressin. The animals were decapitated in one hour. Oxygen absorption by mitochondria of the heart in oxidation of 2.5-10 mM of the succinate increased by 90-120%, as compared to control. Stimulation of respiration by ADP was decreased 1.5-2 times. Simultaneous administration of the succinate and glutamic acid normalized the respiration and phosphorylation. A possibility of inhibition of succinic-dehydrogenase by the oxalo-acetic acid was suggested. Switching of respiration to succinic acid and limiting of the SDG activity can be considered as adaptive factors under conditions of changes in rheological properties of the blood, and are directed to the maintenance of cardiac activity, this being evidenced by the absence of changes in the ATP-asic activity and in the myosin content of the heart.
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PMID:[The influence of rheologic properties of the blood on adaptive processes in the myocardium]. 12

The NH exchange rates in aqueous media of oxytocin and 8-lysine vasopressin (LVP) have been measured by using transfer of solvent saturation method. The data are consistent with a "highly motile" dynamic equilibrium between folded and highly solvated conformations. The highly-motility limit applies to the exchange of NH hydrogens of oxytocin and LVP. Folded structures are more prevalent in oxytocin than in LVP. Partial shielding is indicated for peptide hydrogens of Asn5 and perhaps also Cys6 of oxytocin and for Cys6 of LVP. It is tentatively proposed that the folded conformation of oxytocin in aqueous media may contain a parallel beta-structure in the tocinamide ring consisting of two hydrogen bonds: one between the Tyr2 C = O and Asn5 peptide NH as originally proposed for the preferred conformation of oxytocin in dimethyl sulfoxide (D. W. Urry and R. Walter), and the second between he Cys1 C = O and the Cys6 NH. In LVP the hydrogen bond between the Tyr2 C = O and Asn5 peptide NH appears to be absent. The acylic tripeptide sequences (-Pro-X-Gly-NH2) of both hormones appear to be predominantly solvated. The second-order rate constants for acid catalyzed exchange of the primary amide hydrogens of Gln4, Asn5, and Gly9 of oxytocin are consistently greater for the trans NH than for the corresponding cis NH. This observation can be rationalized in terms of mechanisms involving protonation of either the amide oxygen, or the amide nitrogen, but with limited rotation about the C - N bond.
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PMID:Amide hydrogen exchange rates of peptides in H2O solution by 1H nuclear magnetic resonance transfer of solvent saturation method. Conformations of oxytocin and lysine vasopressin in aqueous solution. 26 22

Experimental studies relating to the direct peripheral vascular actions of neurohypophyseal hormones and their synthetic variants are reviewed. In addition, the available data on the comparative pharmacologic actions of these peptides on mammalian vascular smooth muscle are reviewed. Experiments relating to mechanisms by which neurohypophyseal peptides induce contraction of blood vessels are discussed. Neurohypophyseal peptide hormones appear to be able to contract and relax vascular smooth muscle, the exact type of response being dependent on species, vascular bed, and region within a vascular bed. Receptors that subserve both contraction and relaxation may exist on different blood vessels within a species, with a preponderance of receptors that subserve contraction being present in most blood vessels. Concentrations of vasopressin that can be considered physiologic (i.e., 10(-13) to 10(-11) M) are capable of evoking responses on a variety of microscopic as well as large blood vessels. Arginine-vasopressin appears to be, relatively, the most potent contractile substance on rat blood vessels investigated to date; angiotensin is not. Preservative-free oxytocin is a contractile agent on all mammalian arterial and arteriolar vessels so far investigated. A great deal of the controversy surrounding the exact vascular actions elicited by these peptide hormones can be attributed to many factors that were not controlled in older experiments. Moreover, rat pressor assays cannot be utilized to determine structure-activity relationship for neurohypophyseal peptides on vascular smooth muscles. Nuerohypophyseal peptide-induced contractions of vascular smooth muscles can be markedly affected by sex, sex hormones, alcohols, [Ca2+]0, [mg2+]0, oxygen deficit, and glucose-deprivation. Extracellular sodium and potassium ions appear to play relatively little role in vasopressin-induced contractions of rat arterial smooth muscle. The terminal amino group, phenolic hydroxyl, aromatic ring and basicity in positions 1, 2, 3, and 8, respectively, of the neurohypophyseal hormones are important for optimizing hormone-receptor affinity and intrinsic contractile activity on vascular smooth muscle. Basicity in position 8 of these peptide hormones is not an absolute requirement for contractile activation of these smooth muscles. Alterations in molecular structure can result in neurohypophyseal peptides with unique, and selective, microcirculatory effects that may be beneficial in the treatment of low-flow states.
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PMID:Vascular smooth muscle and neurohypophyseal hormones. 32 65

Plasma vasopressin concentrations were estimated in twelve patients undergoing cardio-pulmonary bypass for open heart surgery. In six patients anaesthesia was maintained with 66% nitrous oxide in oxygen, whilst the remaining six additionally received halothan as a vasodilator during the bypass period. Induction of anaesthesia had little effect on plasma vasopressin concentrations, whilst marked increases were seen during surgery and bypass in both groups of patients. However, in those patients receiving halothane, significantly higher concentrations were reached, a maximun b36.1 +/- 8.9 (SEM) muu/ml being seen in contrase to 15.4 +/- 2.2 muu/ml in the group receiving nitrous oxide in oxygen alone.
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PMID:The effects of halothane on plasma vasopressin during cardio-pulmonary bypass. 32 88

The authors determined cardiovascular, renal, and hormonal responses to increased airway pressure during continuous positive-pressure ventilation (CPPV) and continuous positive airway pressure (CPAP). Nine healthy, hydrated laboratory swine had appropriate catheters placed to allow for measurement of intrapleural, aortic, inferior vena caval, and left ventricular end-diastolic pressures; cardiac output; and urinary flow. Samples of arterial blood were analyzed for oxygen and carbon dioxide tensions, pH, plasma vasopressin, osmolality, and creatinine and sodium concentrations. Urine was analyzed for osmolality and creatinine and sodium concentrations, and volume was recorded. Intrapleural pressure was subtracted from left ventricular end-diastolic pressure to calculate transmural pressure, a reflection of left ventricular filling pressure. Glomerular filtration rate and urinary free-water and osmolal clearances were also calculated. Expiratory left ventricular filling pressure was decreased equally by CPAP and CPPV. However, inspiratory left ventricular filling pressure and cardiac output were decreased by CPPV only. Urinary flow and glomerular filtration rate were decreased equally by CPAP and CPPV. Sodium excretion was decreased and plasma vasopressin increased by CPPV, but not by CPAP. Urinary free water and osmolal clearances were not changed by either ventilatory pattern. Although many of the renal-function variables were affected similarly by CPPV and CPAP, these alterations were not influenced solely by cardiac output or vasopressin, because only CPPV depressed cardiac output and increased vasopressin levels.
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PMID:Renal function and cardiovascular responses during positive airway pressure. 37 28

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 various doses of intravenous vasopressin on mesenteric arterial blood flow, intestinal oxygen consumption, and cardiac output in anesthetized dogs were investigated. Optimal dose rate of intravenous vasopressin was found to be 3.0 mU/kg/min. At this dose rate, mesenteric arterial blood flow, intestinal oxygen consumption, and cardiac output decreased by 57%, 57% and 26%, respectively. Increasing the dose rate to 8.0 mU/kg/min did not offer significant gains. Maximum effect was observed 20 min after the beginning of the infusion. The effects disappeared 10-20 min after the infusion was discontinued, with the exception of superior mesenteric blood flow which showed a rebound increase. We conclude that in the anesthetized dog, intravenous infusions of vasopressin at low dose rates (3.0 mU/kg/min) substantially reduce mesenteric blood flow and intestinal oxygen extraction with moderate reduction of cardiac output. Possible clinical applications of low dose intravenous infusions of vasopressin would include reduction of portal hypertension and bowel protection during radiation therapy.
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PMID:Effects of intravenous vasopressin on canine mesenteric arterial blood flow, bowel oxygen consumption, and cardiac output. 41 36

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

Cardiorespiratory, thermal, and renal responses to a 30-min head-out immersion in 15 degree C water were studied at 1-ATA air and 11-ATA helium-oxygne environments in four male subjects wearing dry suits. Cardiorespiratory responses to immersion (reductions in heart rate, expiratory reserve volume, vital capacity, and thoracic impedance; and increases in stroke volume, cardiac output, and inspiratory capacity) were comparable at both pressures. However, thermal responses to immersion (a reduction in mean skin temperature and increases in skin heat flux and suit conductance) were significantly greater at 11 ATA compared to those at 1 ATA. The rate of urinary excretion of norepinephrine increased significantly during and after immersion at 11 ATA but not at 1 ATA. In contrast, the urinary excretion of epinephrine was not altered by pressure or immersion. The immersion diuresis was greater and lasted longer at 11 ATA than at 1 ATA although there was no difference in the endogenous creatinine excretion . This diuresis was accompanied by a significant natriuresis which was more marked at 1 ATA than at 11 ATA. At 1 ATA, the urinary excretion of both aldosterone and antidiuretic hormone (ADH) decreased during immersion. At 11 ATA, the rate of excretion of these hormones before immersion was lower compared to that at 1 ATA and did not change significantly during immersion. These results indicate that immersion in a hyperbaric helium-oxygen environment presents a greater cold stress than at 1-ATA air, and also that immersion diuresis and natriuresis at high pressure may be induced by a factor other than inhibition of aldosterone and ADH.
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PMID:Physiological responses to head-out immersion in water at 11 ATA. 63 73

Eight men, 19-35 years of age, breathed 20.9% (normal oxygen), 13.9% (mild hypoxia) or 11.1% (severe hypoxia) oxygen in nitrogen gas mixtures during three 20 min periods, which were separated by 1 h recovery periods. The order in which the gas mixtures were breathed was random. The partial pressure of oxygen decreased from a mean of 93.5 during exposure to normal oxygen to 53.9 and 36.7 mmHg during mild and severe hypoxia respectively. There were corresponding decreases in haemoglobin saturation. The partial pressure of carbon dioxide was lower and the pH higher during severe hypoxia than during exposure to normal oxygen. There were no changes in the plasma osmolality or in the concentrations of sodium or potassium in the plasma. There was a tendency for both the renin activity and the concentration of aldosterone in the plasma to decrease progressively as the percentage of oxygen breathed decreased. Unlike severe hypoxia, mild hypoxia suppressed the concentration of antidiuretic hormone (ADH) in the plasma of all subjects by about 59%; during severe hypoxia the reduction was not significant, being only about 33%. These data are consistent with the suggestion that the effect of hypoxia on the release of ADH is dependent on the level of hypoxia.
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PMID:Response of antidiuretic hormone to acute exposure to mild and severe hypoxia in man. 66 35


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