Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelets were examined to enable a simultaneous investigation to be made of indolylamine and electrolyte metabolism in affective disorder. No significant differences were detected in either platelet membrane ATPase or adenyl cyclase specific activity in any of the groups of patients studied, when compared with appropriate controls. A reduced Vmax and y for the 5-hydroxy-tryptamine uptake process into platelets was observed in both unipolar and bipolar depressed groups. The Km for this process was not significantly different in any of the patients from that found in control subjects. Lithium therapy was shown not to influence significantly any of the platelet parameters examined. It is suggested that membrane enzyme changes found in some peripheral cells in patients suffering from affective disorder, i.e. reduced Na+ + K+ - ATPase activity in erythrocytes in depression, is not common to all peripheral cells and may or may not reflect central nervous system changes.
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PMID:Studies on human blood platelets in affective disorder. 15 82

The effects of ether, chloroform, and halothane on calcium accumulation and ATPase activity of rat heart microsomes and mitochondria as well as on myofibrillar ATPase activity were investigated. Chloroform and halothane depressed microsomal and mitochondrial calcium uptake and binding in a parallel fashion. Ether decreased microsomal calcium binding and mitochondrial calcium uptake to varying degrees, while mitochondrial calcium binding was slightly enhanced. Whereas ether had no effect, chloroform depressed microsomal and mitochondrial total APTase activities and halothane decreased microsomsl ATPase and slightly stimulated mitochondrial total ATPase activities. Halothane was found to depress myofibrillar Mg2+-ATPase and ether was capable of decreasing myofibrillar Ca2+-ATPase. Chloroform was seen to inhibit both myofibrillar enzymes. These results suggest that the cardiodepressant actions of volatile anesthetic agents may be due to alterations in the calcium accumulating abilities of microsomal and mitochondrial membranes while direct myofibrillar effects may contribute to the depression seen with relatively higher concentrations of anesthetics.
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PMID:Subcellular effects of some anesthetic agents on rat myocardium. 15 65

In experiments on isolated gallbladders (GB) of frogs it was established that noradrenaline in concentration of 6.10(-9)--3.10(-4) M acting on the organ from the serosalsurface causes firstly a short increase and then -- a prolonged inhibition of the absorption rate of NaCl -- isotonic fluid from the gall bladder cavity. While the concentration of the mediator increases in the inculation medium, its inhibiting effect increases too. Depression, and at high concentration in the medium, full inhibition of the process of fluid absorption is accompanied with distinct decrease of Na--, K--ATPase activity of gall bladder epithelial cells. Mediator in concentration of 3.10(-8) M caused an increase of membrane potential of the epithelial cells, while its increasing in the inculation medium to 3.10(-6) M caused a decrease of the transmembrane potential difference. Under the noradrenaline influence the increase of the osmotic permeability of the gall bladder's wall for the water flow directed from the mucosa to the serosalsurface of the organ took place, and also the decrease of the wall's permeability for the water flow in the opposite direction was seen. It was concluded that the noradrenaline inhibitory action on the process of absorption of NaCl--isotonic fluid from the gall bladder cavity was observed because of the decrease of the Na--K--ATPase activity, and also because of the change of the permeability of epithelium for the passive ion and water transport.
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PMID:[Effect of noradrenaline on ion and water transport through frog gall bladder epithelium]. 15 53

Post-tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug-free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion-selective microelectrodes. The post-stimulation clearing of [K+]0 was not accelerated by phenytoin, and frequently it was slowed. Post-stimulus undershooting of [K+]0 was diminished. Oxidation of NADH in cortex and of cytochrome a, a3 in spinal cord were measured by optical methods. Stimulus-evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+-K+-activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of "resting" redox levels of respiratory enzymes. The local regulation of blood flow remained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus-evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to a lesser exchange of ions.
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PMID:Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord. 19 41

Effects of vanadate on ouabain binding and inhibition of sodium and potassium adenosine triphosphatase (Na+ + K+)-ATPase) were investigated under various ionic conditions. 1. Vanadate facilitated ouabain binding to (Na+ + K+)-ATPase in the presence of Mg2+ and this facilitation was partially reversed by catechol. 2. Vanadate antagonized the ability of high concentrations of NaCl to inhibit ouabain binding in the presence of magnesium. 3. Ouabain binding to the vanadate-enzyme complex, formed from magnesium and vanadate, was more sensitive to depression by potassium than that to the phosphoenzyme formed from magnesium and inorganic phosphate. 4. Preincubation of (Na+ + K+)-ATPase with vanadate in the presence of magnesium initially formed a potassium-insensitive complex as shown by a rapid initial rate of ouabain binding. However, within 5 min potassium overcame the vanadate potentiation of ouabain binding regardless of the order in which it was added to the reaction mixture. 5. Under conditions of enzyme turnover, vanadate failed to antagonize the inhibitory power of ouabain despite the presence of a high concentration of potassium. This suggests a possible relationship between the sensitivity of the sodium pump in various tissues to the cardiac glycosides and intracellular vanadate concentrations.
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PMID:Effects of vanadate on ouabain binding and inhibition of (Na+ + K+)-ATPase. 22 60

A phytohemagglutinin extract is prepared from raw kidney beans (Phaseolus vulgaris) and incorporated at a level of 1% (dry matter) in the diet of young growing rats. Beside a decrease of feed intakes, the main effects of the experimental diet are the following : growth depression, decrease of dry matter and protein digestibility and hypoglycemia. Biological value, organs weight (liver, kidneys, spleen) did not change significantly. The hemagglutinin extract induces an inhibition of saccharase activity whereas (Na+-K+)-ATPase remains unchanged. Growth depressing effect may be due to an alteration of hydrolysis and absorption mechanisms at the level of brush border of enterocytes.
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PMID:[Effects of a phytohemagglutinin extract on growth, nitrogen digestibility and the activity of invertase and (Na+-K+)-ATPase in the intestinal mucosa of the rat]. 23 10

The actions of thromboxane B2 on various parameters of cardiac performance were studied using the isolated perfused rat heart model. In concentrations from 100 pg/ml to 1 microgram/ml TXB2 significantly reduced the total generated myocardial contractile force. These changes were usually associated with an increase in the coronary perfusion pressure indicating an elevated coronary vascular resitance. Significant coronary pressure alterations were seen with TXB2 concentrations between 1 ng/ml and 1 microgram/ml. No significant changes were seen in either the resting tension or heart rate after TXB2 administration. However TXB2 (10 pg/ml to 10 ng/ml,, significantly reduced the amplitude of the electrical activity as observed in R wave changes of the surface electrocardiogram recording. In another series of experiments the action of TXB2 on rat heart sarcolemmal ATPase activity was studied. TXB2 significantly reduced the activity of the MG++ dependent - Na+ - K+ stimulated ATPase (Na+ - K+ ATPase) in these membrane preparations in concentrations from 10 ng/ml to 1 microgram/ml. Kinetic studies demonstrated that TXB2 reduced Vmax and increased the concentration required of ATP, Na+ and K+ for half-maximal enzyme activity. TXB2 did not inhibit either Ca++ or ouabain-induced depression of Na+ - K+ ATPase activity. The activity of either Mg++ or Ca++ - stimulated ATPase was not affected by TXB2. These results suggest possible important actions of TXB2 on rat heart activity which may be related to Na+ - K+ ATPase inhibition.
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PMID:Thromboxane B2: a cardiodepressant of isolated rat hearts and inhibitor of sarcolemma Na+ - K+ stimulated ATPase activity. 23 17

We present evidence in accord with the observations of S. Kalsner (Br. J. Pharmacol. 36: 582-593, 1969) that in the rabbit aorta, desoxycorticosterone (DOC) potentiates the contractile response to certain catecholamines by inhibiting their degradation by catechol-O-methyltransferase. In contrast, DOC depresses the contractile responses in rat aorta and tail arteries. To elucidate the mechanism of this depression the effect of DOC was evaluated under various conditions. DOC depressed the contractile response to epinephrine, phenylephrine, KCl, and angiotensin II. The depression was unaltered by ouabain or by a potassium-free solution, indicating that DOC did not produce its depression by altering Na-K-ATPase activity. The depression is unaltered in a chloride-free solution, demonstrating that the DOC effect is not caused by a change in membrane permeability to chloride. Radioisotope studies demonstrate that DOC does not alter membrane permeability to potassium. Removal of extracellular calcium with EGTA (ethylene glycol-bis (beta-aminoethyl ether) N, N'-tetraacetic acid) significantly reduced the magnitude of the DOC depression. Indirect evidence is presented suggesting that DOC might increase calcium binding to the plasma membrane, resulting in its stabilization and hence in a depression of the contractile response.
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PMID:In vitro effects of desoxycorticosterone on vascular smooth muscle. 46 13

Interactions between some substances (theophylline, noradrenaline, imidazole, ouabain and verapamil) and adenosine or adenosine triphosphate (ATP) were examined by recording the twitch tension of partially magnesium blocked phrenic-rat diaphragm preparations stimulated indirectly. Theophylline (an inhibitor of phosphodieterases) prevented and reversed the neuromuscular depression induced either by adenosine or ATP, and these substances antagonized the neuromuscular facilitation caused by imidazole (an activator of phosphodiesterases); noradrenaline and ouabain did not modify and verapamil increased that depression. These results indicate that the putative purine presynaptic receptor is not the ATPase, that it does not appear to operate by implication of cyclic AMP, but that it could mediate a process involved in the reduction of transmitter release by regulating the entry of calcium that follows the depolorization of the motor nerve endings.
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PMID:Purine effects at the neuromuscular junction and their modification by theophylline, imidazole and verapamil. 47 9

The development of potassium specific ion exchanger microelectrodes has enabled investigators to measure directly brain extracellular potassium ion activity. Although serum potassium in various species ranges between 3.5 and 6 mEq/l, brain extracellular potassium is maintained at a level close to 3 mEq/l independent of fluctuations in serum values. Despite this buffering of the internal brain environment by extracerebral changes, local variations in extracellular potassium occur in response to evoked neuronal activity, seizures, and spreading depression. Mechanisms involved in the maintenance of this ionic homeostasis in the brain include mediated transport at the level of the cerebral capillary and the choroid plexus epithelium. In addition, there are ouabain-sensitive clearance mechanisms presumably involving Na,K-ATPase that participate in the removal of excess potassium. The relative roles of simple diffusion, high glial cell conductance of potassium, and active ionic pumps in restoring basal potassium levels after activity are still controversial.
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PMID:Maintenance of a constant brain extracellular potassium. 77 Jan 98


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