Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 11 conscious normovolaemic patients with acute or chronic pancreatitis the effect of a continuous intravenous infusion of lysine-8-vasopressin, 5 IU/70 kg b.w./20 min on the portal and the hepatic venous blood flows was studied by using multiple portal catheters, oxygen saturation measurements and an indicator dilution technique with continuous infusion of 133Xe into the portal vein or its tributaries. During vasopressin infusion the total hepatic blood flow, estimated by the Bradley technique with indocyanine green dye, was reduced to 61% of the value at rest. Owing to the simultaneously occurring streamlining of the portal venous flow with incomplete mixing of indicator and blood, the portal and hepatic venous blood flows could be measured in only 3 of 9 patients. The reduction in the portal venous blood flow during vasopressin infusion was more marked than the decrease of the total hepatic flow, corresponding to a calculated increase of the hepatic arterial flow of 50%. Total splanchnic oxygen uptake and extrahepatic splanchnic oxygen uptake were unchanged during and after infusion of vasopressin. Thus, changes in splandhnic blood flow could be estimated from changes in arteriovenous oxygen differences. Also by this method a more pronounced reduction in the portal venous than of the hepatic venous blood flow was observed. The decrease during vasopressin infusion of the superior mesenteric venous flow was more marked than that of the splenic vein. The splanchnic circulatory changes may be different for other doses of vasopressin and in cirrhotic patients with higher hepatic arterial blood flow fractions.
 ...
PMID:Effect of vasopressin on regional splanchnic blood flows in conscious man. 126 41

Brain death is associated with loss of hypothalamic, pituitary and brain stem function resulting in apnea, bradycardia and hypotension, poikilothermia, and diabetes insipidus. In order to preserve body functions mechanical ventilation is continued with the aim to maintain an arterial partial pressure of oxygen of more than 100 mmHg. Previous fluid restrictions and the application of diuretics during the treatment of high intracranial pressure frequently result in dehydration. Progressive vasodilation may induce severe hypotension and fluid replacement with cristalloids and if necessary colloids may be called for until the central venous pressure reaches 10 cm H2O. Continuous substitution of potassium and the use of hypotonic solutions such as glucose 5% may avoid hypokalaemia and hypernatraemia, respectively. Inotropic support with dopamine (5-10 micrograms/kg.min) or adrenaline (0.01-0.1 micrograms/kg.min) may be needed to maintain normal mean arterial blood pressure (65 mmHg). Polyuria (5000 ml/24 h) can be treated by continuous intravenous infusion of antidiuretic hormone (0.5-2-10 U/h). Hypothermia must be prevented by warming all fluids (37 degrees C) and covering the patient with heat saving blankets.
 ...
PMID:[Management of the organ donor]. 128 68

The influence of Ca2+ and the possible action of hormone blockers on the activation of glycogenolysis by methotrexate were investigated. Methotrexate was inactive on glycogenolysis and oxygen uptake when the liver, depleted of intracellular Ca2+, was perfused with Ca(2+)-free medium. The action of methotrexate in calcium-depleted hepatocytes could be restored by the addition of extracellular Ca2+. When Ca2+ was absent in the extracellular medium, but the intracellular stores were not depleted, methotrexate produced transient and progressively attenuated increases in glycogenolysis and oxygen uptake. Like many agonists, methotrexate produced transient increases in Ca2+ efflux. The action of methotrexate was not blocked by the antagonists of norepinephrine, phenylephrine, isoproterenol, vasopressin and angiotensin II. It was concluded that methotrexate acts through a Ca(2+)-dependent mechanism, which is similar to that of the Ca(2+)-dependent agonists. This action, however, seems not to be receptor mediated.
 ...
PMID:Activation of glycogenolysis by methotrexate. Influence of calcium and inhibitors of hormone action. 132 84

The dynamic model developed in our previous publications [1,2] was used to calculate the flux control coefficients of oxidation, phosphorylation and proton leak fluxes for isolated mitochondria and for three modes of work of intact cells (hepatocytes). The results obtained were compared with experimental data, especially those measured in the frame of the 'top-down approach' of the metabolic control theory. A good agreement for mitochondria and for intact cells was found. The control of the oxygen consumption flux is shared between the ATP utilization (main controlling factor), substrate dehydrogenation, proton leak and, in some conditions, the ATP/ADP carrier. The phosphorylation subsystem seemed to be controlled mainly by itself, while the proton leak was influenced by all three subsystems. It was also shown that the large relative change in the enzyme activity during inhibitor titration of mitochondria or cells could lead to the overestimation of some flux control coefficient values in experimental measurements. An influence of some hormones (glucagon, vasopressin, adrenaline and others) on the mitochondrial respiration was also simulated. Our results suggest that these hormones stimulate the substrate dehydrogenation as well as the phosphorylation system (ATP usage and, possibly, the ATP/ADP carrier).
 ...
PMID:Theoretical studies on the control of the oxidative phosphorylation system. 132 30

Endothelial cells isolated from the thoracic aorta of normoxic and chronically hypoxic rats were perfused (0.5 ml min-1) and stimulated by increased flow rate (3.0 ml min-1). The release of ATP, endothelin and vasopressin was investigated. During periods of high flow rate, endothelial cells isolated from normoxic rats increased their release of ATP and endothelin. In comparison, in hypoxic rats, ATP release during the period of high flow rate was less, whereas endothelin release was greater. Vasopressin release was not increased during periods of stimulation in either group of animals. These results suggest that, under conditions of reduced arterial oxygen tension, a dynamic balance between ATP and endothelin release could regulate the response of vessels to shear stress.
 ...
PMID:Chronic hypoxia changes the ratio of endothelin to ATP release from rat aortic endothelial cells exposed to high flow. 134 80

Previous experiments have demonstrated that consumption of a glucose polymer-electrolyte (GP-E) beverage is superior to water in minimizing exercise-induced decreases in plasma volume (PV). We tested the hypothesis that elevated plasma concentrations of vasopressin and/or aldosterone above that seen with water ingestion may explain this observation. Six trained cyclists performed 115 min of constant-load exercise (approximately 65% of maximal oxygen consumption) on a cycle ergometer on two occasions with 7 days separating experiments. Ambient conditions were maintained relatively constant for both exercise tests (29-30 degrees C; 58-66% relative humidity). During each experiment, subjects consumed 400 ml of one of the following beverages 20 min prior to exercise and 275 ml immediately prior to and every 15 min during exercise: (1) distilled water or (2) GP-E drink contents = 7% carbohydrate (glucose polymers and fructose; 9 mmol.l-1 sodium; 5 mmol.l-1 potassium; osmolality 250 mosmol.l-1). No significant difference (P > 0.05) existed in mean skin temperature, rectal temperature, oxygen consumption, carbon dioxide production or the respiratory exchange ratio between treatments. Further, no significant differences existed in plasma osmolality and plasma concentrations of sodium, potassium, chloride or magnesium between treatments. Plasma volume was better maintained (P < 0.05) in the GP-E trial at 90 and 120 min of exercise when compared to the water treatment. No differences existed in plasma levels of vasopressin or aldosterone between treatments at any measurement period. Further, the correlation coefficients between plasma concentrations of vasopressin and aldosterone and change in PV during exercise were 0.42 (P < 0.05) and 0.16 (P > 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Fluid replacement beverages and maintenance of plasma volume during exercise: role of aldosterone and vasopressin. 142 51

This study investigated the accuracy of laser-Doppler flowmetry (LDV) and reflectance spectrophotometry (RS) measurements as an index of blood flow in the gastric mucosa of the rat, in experimental conditions such as pharmacologically induced vasoconstriction, hypoxia, hyperoxia, and acute normovolemic anemia. Hydrogen gas clearance was used as a reference method. After vasopressin infusion, LDV signal and indexes of hemoglobin (IHb) and oxygen (ISO2) content in the gastric mucosa estimated by RS significantly decreased in parallel with the reduction of gastric mucosal blood flow (GMBF). Neither hypoxia (5% O2 administration) nor hyperoxia (100% O2) affected GMBF or LDV signal. However, both IHb and ISO2 significantly decreased or increased after hypoxia or hyperoxia, respectively. Acute normovolemic anemia induced a significant increase in GMBF, while LDV signal and ISO2 remained unchanged. IHb significantly decreased in linear relationship with the decrements in the hematocrit. It is concluded that 1) in pharmacologically induced GMBF changes, LDV and RS correlate with GMBF; 2) when changes in hemoglobin saturation are induced, LDV but not RS reflects GMBF; and 3) in acute normovolemic anemia, neither LDV nor RS reflects changes in GMBF.
 ...
PMID:Limitations of laser-Doppler velocimetry and reflectance spectrophotometry in estimating gastric mucosal blood flow. 821 80

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.
 ...
PMID:[Pathophysiology, prevention and therapy of altitude pulmonary edema]. 149 42

The effects of vaso-active agents on hepatic function and splanchnic oxygenation were studied in 17 patients with cirrhosis and portal hypertension. Eight patients received vasopressin (0.3 iu/min) and nine patients received nitroglycerin (50 micrograms/min). Both drugs caused a significant reduction in the portal venous pressure gradient. Vasopressin infusion significantly decreased intrinsic clearance of indocyanine green (-23%, P less than 0.01). This may be due to a decreased hepatic perfusion (-28%, P less than 0.01) and portal venous oxygenation (-15% in portal venous oxygen tension, P less than 0.05). In contrast, no changes in hepatic perfusion and portal venous oxygenation were observed after nitroglycerin infusion. Nitroglycerin did not decrease intrinsic clearance of indocyanine green. These results suggest that vasodilators, rather than vasoconstrictors, might be welcome in the treatment of patients with cirrhosis and portal hypertension.
 ...
PMID:Effects of vaso-active agents on hepatic function and blood gases in patients with cirrhosis: a study of vasopressin and nitroglycerin. 157 96

The effects were investigated of the choleretic bile salt glycoursodeoxycholate (G-UDCA) and of the cholestatic bile salt taurochenodeoxycholate (T-CDCA) on changes in perfusate Ca2+, glucose and oxygen and in bile calcium and bile flow induced by the administration of (a) vasopressin, (b) glucagon and (c) glucagon plus vasopressin together to the perfused rat liver [Hamada, Karjalainen, Setchell, Millard & Bygrave (1992) Biochem. J. 281, 387-392]. G-UDCA itself increased the secretion of calcium in the bile several-fold, but its principal effect was to augment each of the above-mentioned metabolic events except glucose and oxygen output; particularly noteworthy was its ability to augment the 'transients' in bile calcium and bile flow seen immediately after the administration of vasopressin with or without glucagon. T-CDCA, by contrast, produced opposite effects and attenuated all of the parameters measured, and in particular the transients in bile calcium and bile flow. The data provide evidence of a strong correlation between calcium fluxes occurring on both the sinusoidal and the bile-canalicular membranes and that all are modifiable by glucagon, Ca(2+)-mobilizing hormones and bile salts.
 ...
PMID:Acute effects of cholestatic and choleretic bile salts on vasopressin- and glucagon-induced hepato-biliary calcium fluxes in the perfused rat liver. 157


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>