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)

1. Homogenates of neural lobes of bovine pituitary glands were fractionated by differential and density-gradient ultracentrifugation and the distribution of adenosine triphosphatase (ATPase) activity was studied. It was shown that all the activity was membrane-bound. 2. On the basis of ionic requirements the ATPase activity was grouped into three categories: (a) Mg(2+)-dependent, (b) Ca(2+)-dependent and (c) Mg(2+)+Na(+)+K(+)-dependent (ouabain-sensitive) ATPases. The activity in the absence of bivalent cations was negligible. The ratio between the activities of the three ATPases varied between the different subcellular fractions. 3. Preincubation of the subcellular fractions with deoxycholate increased the activity of the Mg(2+)+Na(+)+K(+)-dependent enzyme, whereas the Mg(2+)- and Ca(2+)-activated ATPases were either unaffected or slightly inhibited. Triton X-100 solubilized the Mg(2+)- and Ca(2+)-ATPases; however, the activity of the Mg(2+)+Na(+)+K(+)-ATPase was abolished by the concentration of Triton X-100 used. 4. All the subfractions displayed unspecific nucleotide triphosphatase activity towards GTP, ITP and UTP. These substrates inhibited the hydrolysis of ATP by all three ATPases. ADP also inhibited the ATPases. 5. Polyacrylamide-gel electrophoresis of extracts containing the Mg(2+)- and Ca(2+)-dependent ATPase activity solubilized by Triton X-100 revealed the presence of two enzymes; one activated by either Mg(2+) or Ca(2+) and the other activated only by Ca(2+). 6. In sucrose density gradients the distribution of vasopressin was different from that of all three types of ATPases. It is therefore suggested that the neurosecretory granules do not possess ATPase activity.
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PMID:Adenosine triphosphatase activity in the neural lobe of the bovine pituitary gland. 428 6

1. In the isolated rabbit ear vascular bed, perfused with Krebs solution, prostaglandins E(1) and F(2alpha) produce dose-dependent, phentolamine-sensitive constrictions.2. These are absent if the animal is pre-treated with reserpine or if the ear is denervated in advance.3. If noradrenaline or vasopressin is added to the Krebs solution, vascular resistance is high and PGE(1) and PGF(2alpha) produce vasodilatation which is unaffected by hyoscine or propranolol.4. Perfusion with theophylline, with added ATP, ADP or 3'5'-AMP, or pre-treatment of the animal with stilboestrol antagonizes the dilator response to PGE(1) in the presence of noradrenaline, which may be reversed. Most of the responses to PGF(2alpha) are reversed. These treatments elevate the level of 3'5'-AMP in tissues.5. It is postulated that prostaglandins exert a regulatory action on 3'5'-AMP levels through inhibition of adenyl cyclase and/or phosphodiesterase and that the resulting rising or falling level of 3'5'-AMP determines the nature of the response by the smooth muscle to the released noradrenaline.
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PMID:The actions of prostaglandins E 1 and F 2 on the on the perfused vessels of the isolated rabbit ear. 433 86

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

A chemically stable carboprostacyclin analogue, ZK 36374 has been compared with two other prostacyclin derivatives with respect to ADP-induced in vitro aggregation of baboon and human platelets and ex vivo platelet aggregation in the baboon. ZK 36374 was also tested on the systemic arterial blood pressure of the baboon and against vasopressin-induced ECG changes in primates. Compared to the other two compounds, ZK 36374 displayed enhanced anti-platelet aggregating activity; there was dissociation between this property and its hypotensive potency. ZK 36374 antagonized the vasopressin-induced ECG changes. These results indicate that ZK 36374 possesses therapeutic potential in vascular disease including that affecting the coronary vessels.
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PMID:Inhibition of platelet aggregation and antagonism of vasopressin-induced ECG changes in primates by a carboprostacyclin analogue, ZK 36374. 620 Sep 48

Content of adenosine phosphate, creatine phosphate, Pi, lactate and ATPase activity were studied in brain of 8-10- and 25-27-months old rats. Content of ATP and ADP and the Na+, K+-ATPase activity were decreased while the level of Pi was increased in rat brain cortex during ageing. Administration of vasopressin caused an increase in lactate, Pi and Na+, K+-ATPase activity, whereas creatine phosphate decreased in the adult rat hypothalamus. Changes in energy metabolism were more pronounced in old rats: simultaneously with the decrease in creatine phosphate and more marked, as compared with adults, increase in Pi and lactate, the content of ATP decreased, ADP and AMP - increased and the Na+, K+-ATPase was distinctly activated in stem and brain cortex.
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PMID:[Effect of vasopressin on energy metabolism of the brain in adult and aged rats]. 624 74

ADP, adrenaline and vasopressin interact positively as agonists in aggregating human blood platelets in vitro. This interaction is maximal if the addition of two of the agonists is separated by 10--20 s but decreases rapidly at longer intervals especially at low agonist concentrations. The agonist concentrations at which positive interaction gives full aggregation are significantly less than those required for such a response to each agonist alone. The lowest concentrations at which adrenaline and vasopressin interact positively are at least two orders of magnitude greater than the normal blood concentrations of these hormones, and at least an order of magnitude greater than the concentrations achieved in pathological states. Specifically antagonizing the adrenaline and ADP receptors showed that the response was to the second agonist added to the system. An inhibitor of intracellular Ca2+ movement (tetracaine) is equally effective in blocking the responses generated by a single agonist or by interaction of two agonists. Inhibitors which increase cyclic-3',5'-AMP concentration (adenosine, prostaglandin E1, dipyridamole) are more effective against the response to a single agonist than that to agonist interaction. These data suggest that positive agonist interaction results from effects on the concentrations of second messengers within the platelet rather than from a direct interaction on the membrane receptors or the transmembrane coupling mechanisms.
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PMID:Positive interaction between agonists in the aggregation response of human blood platelets: interation between ADP, adrenaline and vasopressin. 624 13

The effect of acute insulin treatment of hepatocytes on pyruvate carboxylation in both isolated mitochondria and cells rendered permeable by filipin was examined. Challenging the cells with insulin alone had no effect on either the basal rate of pyruvate carboxylation or gluconeogenesis, although it did suppress the responses to both glucagon and catecholamines. Insulin treatment was unable to antagonize the enhanced rate of pyruvate carboxylation caused by stimulation of the cells with either angiotensin or vasopressin. Neither insulin nor the gluconeogenic hormones altered the total extractable pyruvate carboxylase activity in the isolated mitochondria, suggesting that the effect of hormones at the level of the isolated intact organelle was mediated via alterations in the intramitochondrial concentrations of effector molecules, notably ATP and the [ATP]/[ADP] ratio and substrate availability. The alterations in pyruvate carboxylation correlate well with glucose synthesis in terms of sensitivity to effector molecules, putative second messengers and time of onset of the response, indicating that alterations in the flux through this enzyme are compatible with it being an important site in the control of gluconeogenesis from C3 precursors.
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PMID:Regulation of mitochondrial pyruvate carboxylation in isolated hepatocytes by acute insulin treatment. 631 Nov 85

[(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

The effect of synthetic 8-arginine vasopressin (vasopressin) was studied in isolated canine basilar, left circumflex coronary, and femoral arteries of the dog. Vascular rings with and without endothelium were suspended for isometric tension recording in physiological salt solution. The removal of the endothelium was confirmed by the absence of relaxations induced by either thrombin (basilar arteries) or acetylcholine (coronary and femoral arteries). In the basilar artery, vasopressin induced concentration-dependent inhibition of myogenic tone. In basilar and coronary arteries, the hormone caused concentration-dependent relaxations during contractions evoked by prostaglandin F2 alpha. In femoral arteries, vasopressin caused contraction. After removal of the endothelium, the inhibitory responses to vasopressin were abolished in basilar arteries and significantly reduced in left circumflex coronary arteries. The contractions of femoral arteries were not affected by endothelium removal. The V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP prevented the inhibitory response to vasopressin, but did not alter endothelium-dependent relaxations of basilar arteries caused by adenosine diphosphate. These results demonstrate that the endothelial cells mediate relaxation induced by vasopressin via specific V1-vasopressinergic receptors.
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PMID:Vasopressin causes endothelium-dependent relaxations of the canine basilar artery. 648 82

Enzymatically prepared split frog skins consisted purely of epithelial cells. Electrical parameters and the cell contents of ATP, ADP, phosphocreatine (PCr), creatine, inorganic phosphate, protein, and water were measured in skins maintained at room temperature. Studies were conducted under base-line conditions, 15 and 60 min after adding vasopressin, and 30 min after adding amiloride. Intracellular ionic activities and concentrations were obtained from previous results. The data demonstrated that 1) the base-line concentration ratio of PCr/ATP was 0.53 +/- 0.03; 2) the average molar free energy of hydrolysis of intracellular ATP was approximately 15.0 kcal X mol-1 under control conditions, changing by less than or equal to 3% with changes in transport; and 3) the free energy of extruding 3 mol of Na+ and accumulating 2 mol of K+ was approximately 9.8 kcal X mol-1 under base-line conditions; the difference between the molar free energies of ATP hydrolysis and of transport work remained large, despite large changes in transepithelial transport. The simplest conclusion is that the Na+ pump of frog skin operates far from equilibrium.
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PMID:Bioenergetics of Na+ transport across frog skin: chemical and electrical measurements. 660 84


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