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)

Jakobs, Bauer & Watanabe [(1985) Eur. J. Biochem. 151, 425-430] reported that treatment of platelets with phorbol 12-myristate 13-acetate (PMA) prevented GTP- and agonist-induced inhibition of adenylate cyclase in membranes from the platelets. This was attributed to the phosphorylation of the inhibitory guanine nucleotide-binding protein (Gi) by protein kinase C. In the present study, the effects of PMA on cyclic [3H]AMP formation and protein phosphorylation were studied in intact human platelets labelled with [3H]adenine and [32P]Pi. Incubation mixtures contained indomethacin to block prostaglandin synthesis, phosphocreatine and creatine kinase to remove ADP released from the platelets, and 3-isobutyl-1-methylxanthine to inhibit cyclic AMP phosphodiesterases. Under these conditions, PMA partially inhibited the initial formation of cyclic [3H]AMP induced by prostaglandin E1 (PGE1), but later enhanced cyclic [3H]AMP accumulation by blocking the slow decrease in activation of adenylate cyclase that follows addition of PGE1. PMA had more marked and exclusively inhibitory effects on cyclic [3H]AMP formation induced by prostaglandin D2 and also inhibited the action of forskolin. Adrenaline, high thrombin concentrations and, in the absence of phosphocreatine and creatine kinase, ADP inhibited cyclic [3H]AMP formation induced by PGE1. The actions of adrenaline and thrombin were attenuated by PMA, but that of ADP was little affected, suggesting differences in the mechanisms by which these agonists inhibit adenylate cyclase. sn-1,2-Dioctanoylglycerol (diC8) had effects similar to those of PMA. The actions of increasing concentrations of PMA or diC8 on the modulation of cyclic [3H]AMP formation by PGE1 or adrenaline correlated with intracellular protein kinase C activity, as determined by 32P incorporation into the 47 kDa substrate of the enzyme. Parallel increases in phosphorylation of 20 kDa and 39-41 kDa proteins were also observed. Platelet-activating factor, [Arg8]vasopressin and low thrombin concentrations, all of which inhibit adenylate cyclase in isolated platelet membranes, did not affect cyclic [3H]AMP formation in intact platelets. However, the activation of protein kinase C by these agonists was insufficient to account for their failure to inhibit cyclic [3H]AMP formation. Moreover, high thrombin concentrations simultaneously activated protein kinase C and inhibited cyclic [3H]AMP formation. The results show that, in the intact platelet, the predominant effects of activation of protein kinase C on adenylate cyclase activity are inhibitory, suggesting actions additional to inactivation of Gi.
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PMID:Effects of activation of protein kinase C on the agonist-induced stimulation and inhibition of cyclic AMP formation in intact human platelets. 244 6

Acute myocardial ischemia (intravenous 0.2 U/kg vasopressin infusion) is shown to cause various changes in the creatine kinase isoenzyme activity: it decreases in mitochondria and sarcoplasmic reticulum and increases in myofibrils and cytosol, no significant alterations taking place in sarcolemma. It may be suggested that the stated changes are important components of the complex adaptational reactions which occur in the ischemic myocardium and support its main contractional function.
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PMID:[Creatine kinase in subcellular components of the rabbit myocardium during experimental obstruction of the coronary circulation]. 343 85

Experiments were conducted on rabbits under conditions of acute restriction of coronary blood flow (intravenous injection of vasopressin in a dose of 0.5 U/kg) and preliminary administration (1 h before vasopressin) of PP-256-Na antioxidant preparation. The activity of creatine kinase isoenzymes bound with sarcoplasmic reticulum and mitochondria membranes were studied as well as the content of diene conjugates in these membranes and accumulation of malonic dialdehyde. It is shown that an essential decrease in the enzyme activity in the membranes occurs against a background of a considerable increase in the content of diene conjugates and accumulation of malonic dialdehyde. A preliminary administration of the antioxidant produces a pronounced protective effect on the enzyme activity.
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PMID:[Relation between the impairment of creatine kinase activity and lipid peroxidation in the membranes of heart mitochondria and sarcoplasmic reticulum in experimental ischemia]. 394 21

[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
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PMID:Cardioprotective action of the new stable epoprostenol analogue CG 4203 in rat models of cardiac hypoxia and ischemia. 644 79

We reported a case of neuroleptic malignant syndrome (NMS) associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 71-year-old woman, who had been diagnosed as hypertension and multiple cerebral infarction, was given sulpiride 150 mg daily for depressive state. Three days after started sulpiride, she developed fever, sweating, difficulty of movement and was admitted to the hospital. The white blood cell count rose to 16,300/mm3 and serum creatine kinase (CK) to 3,063 IU/L. Two days later CK rose to 20,050 IU/L regardless of stopping the drug, so she was transferred to our hospital for further investigation. On admission, it was the 6th day from the onset, she was mute and akinetic accompanied by muscle pain and rigidity in extremities. Serum CK was 1,831 IU/L, Na 122 mEq/L, osmolality 244 mOsm/kg, plasma antidiuretic hormone (ADH) level 6.5 pg/ml and urine Na was 101 mEq/L, osmolality 467 mOsm/kg. Renal and adrenal functions, plasma renin activity were normal. From the history, course and these data, diagnosis of NMS associated with SIADH was made. Intravenous sodium (130-200 mEq/day) and fluids (1,000-1,200 ml/day) were carefully infused. She became active, muscle pain disappeared and rigidity, akinesia decreased. CK, serum Na and osmolality gradually improved to normal. About the transient increase in ADH secretion, we considered that hypothalamic disturbance in NMS might induce leakage of stored ADH from neuroendocrine neurons in it.
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PMID:[Neuroleptic malignant syndrome associated with the syndrome of inappropriate secretion of antidiuretic hormone]. 778 Dec 36

Exercise-induced hyponatremia is commonly believed to be associated only with extraordinary physical efforts, or particularly strenuous exercise. Hyponatremia complicating moderate exercise has not been described previously. The authors describe the characteristics of seven patients with life-threatening hyponatremia associated with mild to moderate exercise. All patients suffered from nausea, vomiting, agitation, and confusion, appearing during or after moderate physical activity. Grand mal convulsions occurred in five of the patients. In laboratory results, hyponatremia was as low as 115 mEq/L, with a relatively high sodium concentration in the urine. High serum creatine kinase activity levels were found in most of the patients. All patients were discharged in good condition, without neurologic sequela. The authors conclude that hyponatremia is a possible complication of moderate exercise, and not only of endurance sports, and that exercise-induced hyponatremia can produce severe neurologic manifestations. The mechanism of the hyponatremia is unclear, but may be due to a hemodynamically inappropriate stimulus for antidiuretic hormone secretion.
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PMID:Case series: hyponatremia associated with moderate exercise. 861 81

It has been reported that the administration of vasopressin induces myocardial ischaemia in rats, which causes electrocardiographic ST segment alterations according to many authors. But rat electrocardiogram (ECG) lacks ST segment. Consequently it appears important to study the effects of vasopressin in rabbits, which show ST segment present in the ECG. Since cardiac necrosis markers are released in the plasma of humans with myocardial infarction, as well as in a variety of experimental models of myocardial necrosis, it is possible that the same may occur in rabbits with myocardial ischaemia induced by vasopressin. The main aim of this study was to investigate whether the administration of vasopressin causes the appearance of specific myocardial necrosis markers, such as cardiac troponin I, myoglobin or creatine kinase MB (CK MB) in rabbits in the presence or absence of modified ECG profile, and to also verify whether these markers are associated with the alterations in some coagulation parameters, that are known to be induced by vasopressin. As the effects of vasopressin are counteracted by nitric oxide (NO), another aim was to verify whether vasopressin also affects plasma NO levels and whether the administration of a NO donor can reverse these effects. Vasopressin was administered to rabbits and caused ischaemic alterations such as electrocardiographic changes, and significantly increased the levels of plasma cardiac necrosis markers (c-troponin I, myoglobin and CK MB). It also elevated diastolic blood pressure (BP), lowered heart rate (HR), increased procoagulation activity, and lowered plasma NO levels. The appearance of heart necrosis, demonstrated by plasma cardiac necrosis markers in the animals receiving vasopressin, was attributed to a drug-induced increase in vasoconstriction and coagulation activity. The intense vasoconstriction and thrombosis may lead to endothelium necrosis and a consequent drop in NO production. The administration of the NO donor nitroglycerin (NG) in the vasopressin treated animals restored NO values, and was capable of preventing the appearance of the plasma cardiac necrosis markers and altered coagulation values. The protective activity of NG was attributed to NO release, which lowers BP values and counteracts coagulation activity in vasopressin-treated animals. The described procedure may also be proposed for the study of early ischaemic myocardial lesions and the screening of NO donors preventing myocardial damage.
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PMID:Cardiac necrosis markers associated with low nitric oxide levels in the plasma of rabbits after treatment with vasopressin: protective effects of nitroglycerin administration. 1216 41

We have previously shown that myogenesis induction by Arg8-vasopressin (AVP) in L6 rat myoblasts involves a sustained stimulation of type 4 cAMP-phosphodiesterase. In this model, we observed that a transient cAMP generation occurs in the minutes following AVP addition. Evidence suggests that cAMP generation is due to the prostaglandins produced in response to AVP binding to V1a receptors and subsequent activation of phospholipase A2. The early cAMP increase was effective in activating cAMP-dependent protein kinase (PKA) and increasing phosphorylation of CREB transcription factor. Inhibition of PKA by compound H89 prior to AVP addition led to a significant reduction of expression of the differentiation marker creatine kinase, whereas H89 added 1-5 h after AVP had no significant effect. Furthermore, PKA inhibition 24 h after the beginning of AVP treatment potentiated differentiation. This shows that both an early activation and a later down-regulation of the cAMP pathway are required for AVP induction of myogenesis. Because phosphodiesterase PDE4D3 overexpressed in L6 cells lost its ability to potentiate AVP-induced differentiation when mutated and rendered insensitive to PKA phosphorylation and activation, we hypothesize that the early cAMP increase is required to trigger the down-regulation of cAMP pathway through stimulation of phosphodiesterase.
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PMID:A bimodal modulation of the cAMP pathway is involved in the control of myogenic differentiation in l6 cells. 1450 85

Substantial fluid shifts occur during liposuction as wetting solution is infiltrated subcutaneously and fat is evacuated, causing potential electrolyte imbalances. In the porcine model for large-volume liposuction, plasma aspartate aminotransferase and alanine transaminase levels were elevated following liposuction. These results raised concerns for possible mechanical injury and/or lidocaine-induced hepatocellular toxicity in a clinical setting. The first objective of this human model study was to explore the effect of the liposuction procedure on electrolyte balance. The second objective was to determine whether elevated plasma aminotransferase levels were observed subsequent to large-volume liposuction. Five female volunteers underwent three-stage, ultrasound-assisted liposuction. Blood samples were collected perioperatively. Plasma levels of sodium, potassium, venous carbon dioxide, blood urea nitrogen, chloride, and creatinine were determined. Liver function analyte levels were measured, including albumin, total protein, aspartate aminotransferase, and alanine transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase, and total bilirubin. To further define intracellular enzyme release, creatine kinase levels were measured. Mild hyponatremia was evident postoperatively (134 to 136 mmol/liter) in four patients. Hypokalemia was evident intraoperatively in all subjects (mean +/- SEM; 3.3 +/- 0.16 mmol/liter; range, 3.0 to 3.4 mmol/liter). Hypoalbuminemia and hypoproteinemia were observed throughout the study (baseline: 2.9 +/- 0.2 g/dl; range, 2.6 to 3.5 g/dl), decreasing to 10 to 40 percent 24 hours postoperatively (2.0 +/- 0.2 g/dl; range, 1.7 to 2.1 g/dl). Aspartate aminotransferase, alanine transaminase, and creatine kinase levels were significantly elevated after the procedure (190 +/- 47.1 U/liter, 50 +/- 7.7 U/liter, and 11,219 +/- 2556.7 U/liter, respectively) (p < 0.01). Release of antidiuretic hormone and even mildly hypotonic intravenous fluid infiltration have long been known to cause hyponatremia postoperatively. Intraoperative hypokalemia is associated with hypocarbia and respiratory alkalosis and the elevated epinephrine levels observed in the concurrent study. Factors having the greatest initial impact on diminished serum albumin and protein levels postoperatively are redistribution and hemodilution. Subsequent diminished viscosity may significantly affect postoperative hemodynamics. Elevated aspartate aminotransferase, alanine transaminase, and creatine kinase levels are associated with skeletal muscle injury, adipocyte lysis, and/or hepatic damage. Therefore, tissue injury is associated with large-volume liposuction as observed in several cellularly released enzymes. Future clinical studies are required to determine the degree of injury and specific tissues that are damaged or sensitive to mechanical trauma and/or drugs used in large-volume liposuction.
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PMID:Electrolyte and plasma enzyme analyses during large-volume liposuction. 1531 60

The aims of this study were to: (1) evaluate the epidemiology of simultaneous upper gastrointestinal bleeding (UGIB) and myocardial injury using parameters including troponin I (TnI); and (2) investigate the predictive risk factors of this syndrome. One hundred and fifty-five patients (101 men, 54 women; mean age, 64.7+/-10.4 years; range, 38-94 years) at the emergency department (ED) with the major diagnosis of UGIB were included. They underwent serial electrocardiography (ECG) and cardiac enzyme follow-up. Emergent gastroendoscopy was performed within 24 hours in most patients except for those who refused or were contraindicated. Mild myocardial injury was defined as the presence of any of the following: typical ST-T change on ECG, elevated creatine kinase-MB (CK-MB)>12 U/L, or TnI>0.2 ng/dL. Moderate myocardial injury was defined as the presence of any two of the previously mentioned conditions. In total, 51 (32.9%) and 12 (7.74%) patients developed mild and moderate myocardial injuries, respectively. Myocardial injury was more common among patients with variceal bleeding (20/25=80.0%) than those with ulcer bleeding (23/112=20.5%). It could partially be attributed to a higher baseline TnI level in cirrhotic patients. After adjusting for significant risk factors revealed by the univariate analysis, UGIB patients with a history of liver cirrhosis and more than three cardiac risk factors comprised a high-risk group for simultaneously developing myocardial injury. Other factors including age, gender, the color of nasogastric tube irrigation fluid, history of nonsteroidal anti-inflammatory drug use, vasopressin or terlipressin administration, vital signs, and creatinine recorded at the ED were not significant predictors. Those who developed myocardial injury had a longer hospital stay (mean duration, 8.73+/-6.94 vs. 6.34+/-2.66 days; p=0.03) and required transfusion of more units of packed erythrocytes.
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PMID:Predictive risk factors for upper gastrointestinal bleeding with simultaneous myocardial injury. 1728 80


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