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

Changes in blood, serum, and urine parameters that are usually associated with fluid and electrolyte balance were studied in 45 volunteers who ran the 1987 Pittsburgh Marathon. There were 39 males and 6 females. The mean age was 39.3 years. Their mean fluid intake was 1650 cc and the mean finishing time was 4 hours and 1 minute. The race was run in the rain with a temperature of 46 degrees F. When the prerace and postrace values of the runners were compared, significant increases were noted in the serum sodium, potassium, blood urea nitrogen (BUN), creatinine, uric acid, creatine phosphokinase (CPK), protein, plasma renin, vasopressin, and urinary potassium. Significant decreases were found in weight, blood pressure, and urinary sodium. No significant differences were noted in serum chloride, serum glucose, and hemoglobin/hematocrit. The mean weight loss of 1.9 kg was less than weight losses reported in marathons run under warmer conditions.
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PMID:Fluid and electrolyte balance during a cool weather marathon. 269 76

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 on rats and rabbits using models of arrhythmias induced by vasopressin, epinephrine, strophanthin, and CaCl2 showed that antioxidants derived from 1,4-dihydropyridines, dibunol, and alpha-tocopherol possessed antiarrhythmic effects. Administration of these antioxidants decreased the occurrence of extrasystoles, disturbances of atrioventricular conductivity and ventricular fibrillation. These drugs also prevented changes in membrane phospholipid composition, inhibited activation of peroxidation, decreased phospholipase activity, prevented a decrease of Ca2+ ATPase and Ca2+ binding and uptake by sarcoplasmic reticulum, and increased sarcolemmal Na+, K+-ATPase, sarcoplasmic reticulum creatine phosphokinase.
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PMID:Antioxidants as antiarrhythmic drugs. 356 51

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

Synthetic [8-arginine]-vasopressin, [8-lysine]-vasopressin, [8-ornithine]-vasopressin or [2-phenylalanine, 8-lysine]-vasopressin aggregated human platelets in heparinized platelet-rich plasma. The lowest effective concentrations (1-4mU/ml) caused a primary transient aggregation, while higher concentrations also caused a secondary irreversible aggregation. Vasopressin was almost inactive in citrated platelet-rich plasma but caused aggregation in recalcified citrated or native material. Vasopressin also aggregated washed human platelets suspended in buffered saline, if fibrinogen and either Ca2+ or Mg2+ ions were present. Ethylene glycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid inhibited aggregation completely but only after preincubation with the platelets, suggesting that platelet-bound calcium was also required. Phosphocreatine with creatine phosphokinase partially inhibited primary aggregation of platelets by vasopressin and prevented secondary aggregation, which suggests that release of platelet ADP contributed to these processes. Concentrations of vasopressin causing irreversible aggregation released small amounts of 14C from platelets containing serotonin-14C. Platelet aggregation induced by vasopressin was inhibited by adenosine, prostaglandin E1, N6,2'-0-dibutyryl cyclic 3',5'-AMP, caffeine, imipramine, or N-ethylmaleimide. Adenosine and prostaglandin E each inhibited the action of vasopressin much more powerfully than that of ADP and, therefore, cannot act solely by inhibiting the effects of the ADP released. In several respects the effect of vasopressin on blood platelets resembled its action on smooth muscle.
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PMID:Aggregation of human blood platelets by vasopressin. 434 80

[(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

Experiments on rats with acute coronary blood flow restriction (intravenous injection of vasopressin in a dose of 0.5 units/kg) have shown a decrease in the activity of creatine phosphokinase (CPK) and activation of lipid peroxidation in sarcoplasmic reticulum (SPR) membranes. These changes were attended by structural abnormalities in the membrane apparatus of the SPR, primarily on the part of the lipid composition. Pretreatment (1 h before vasopressin) of the animals with the antioxidant AV-156Na averted the development in the SPR membranes of the changes described. This evidences that the rate of peroxide reactions in the myocardium might determine in many respects the metabolic and structural supply of the cell apparatus.
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PMID:[Creatine phosphokinase activity in myocardial sarcoplasmic reticulum membranes in experimental coronary insufficiency]. 685 90

Certain key parameters of energy metabolism in a complex mechanism of energy transport in the myocardium cells were studied in experiments on dogs with dosed limitation of the coronary blood flow (by 90%) as well as in experiments on rabbits with the intravenous injection of vasopressin (0.2 units per 1 kg of mass). Animals of all groups under study revealed essential changes in the content of creatine phosphate and in the activity of creatine phosphokinase as compared with the control groups. A possible role of creatine phosphokinase is discussed in the processes of myocardium function energy supply under conditions of creatine phosphate deficiency during a slightly pronounced ischemia.
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PMID:[Components of the creatine kinase system in the myocardium with experimental disturbance of coronary blood flow]. 708 Feb 19

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


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