Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amphetamine overcomes the amnesia caused by cycloheximide (CXM) provided it is administered closely following the learning trial. In day-old chickens with one trial passive avoidance learning, there is a short-term, labile memory existing for 90 min following training under the influence of CXM. Amphetamine has been shown to keep the memory at precisely the level exhibited by the labile, cycloheximide-resistant memory trace at the time of injection. Norepinephrine, methoxamine (an alpha adrenergic stimulant) and isoprenaline (a beta adrenergic stimulant) each mimic the amphetamine effect in CXM-pretreated chickens. That the action of amphetamine could be due to its release of norepinephrine is supported by the finding that it could be blocked by both alpha adrenergic (piperoxane) and beta adrenergic antagonists (propranolol). It has been suggested that this labile memory trace depends on the functioning of a sodium pump. Norepinephrine may be modulating memory formation by an action on the sodium pump since in preliminary biochemical assays norepinephrine stimulated the sodium pump (Na+/K+ ATPase) activity in chicken forebrain total homogenate.
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PMID:Modulation of cycloheximide-resistant memory by sympathomimetic agents. 1 May 77

Exposure of rats to an ambient temperature of 5 degrees C for 4 to 6 weeks led to a 30 to 80 percent increase in the rate of oxygen consumption and a 50 percent increase in the rate of ethanol oxidation by liver slices, a 50 percent increase in mitochondrial alpha-glycerophosphate oxidase activity of liver, and a 100 percent increase in Na++K+-activated adenosine-triphosphatase, activity. Ouabain, an inhibitor of the Na++K+-activated adenosine-triphosphatase, completely blocked the extra respiration and ethanol oxidation. Dinitrophenol, which increases oxygen consumption and ethanol oxidation by liver slices from normal rats, was ineffective with slices from cold-exposed animals. Ethanol disappearance rate in vivo was also increased by cold acclimation, even though liver alcohol dehydrogenase activity was reduced. It is suggested that increased hydrolysis of ATP by the sodium pump system is responsible for the increased oxygen consumption and ethanol metabolism in the livers of cold-acclimated animals.
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PMID:Ethanol metabolism and liver oxidative capacity in cold acclimation. 12 85

1. The (Na++K+)-ATPase of red cell membranes is unable to hydrolyse ATP-analogues in which the oxygen atom linking the beta- and gamma-phosphate groups is replaced by a minusCH2minus or minusNH-bridge. 2. In resealed ghosts both these ATP-analogues support K:K exchange but not Na:K exchange. ATP supports both modes of operation of the sodium pump, whereas neither occurs without any nucleotide. 3. These results support the hypothesis that ATP is needed as a cofactor for K:K exchange to occur, and make it extremely unlikely that phosphorylation from ATP is involved.
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PMID:The interaction of ATP-analogues possessing a blocked gamma-phosphate group with the sodium pump in human red cells. 12 51

The relationship between Na+, K+-ATPase inhibition by monovalent cations and their inotropic effect was studied in guinea pig hearts. The activity of partially purified cardiac enzyme was assayed in the presence of 5.8 mM KC1 and either 20 or 150 mM NaCl. Rb+ and Tl+ inhibited Na+, K+-ATPase activity, the magnitude of the inhibition by these cations being greater in the assay media containing lower Na+ concentrations. Tl+ produced a dose-dependent inhibition of Na+, K+-ATPase activity in the presence of 20 mM Na+ and 75 mM K+, a cationic condition similar to that of intracellular fluid. Other monovalent cations such as K+, Cs+, NH4+, Na or Li+ produced essentially no effect on the Na+, K+-ATPase activity or slightly stimulated it. In left atrial strips stimulated with field electrodes and bathed in Krebs-Henseleit solution (5.8 mM K+ and 145 mM Na+), addition of Cs+ failed to alter the isometric contractile force significantly. NH4+ and K+ caused a transient positive inotropic effect which was partially blocked by propranolol. The positive inotropic response to K+ was followed by a negative inotropic response. Rb+ produced a sustained, dose-dependent inotropic response reaching a plateau at 1-2 min, whereas Tl+ produced a dose=dependent positive inotropic effect which developed slowly over a 30-min period. The positive inotropic effects produced by Rb+ and Tl+ were insensitive to propranolol pretreatment. Concentrations of Tl+ and cardiac glycosides which produce similar inotropic effects appear to cause the same degree of Na+-pump inhibition. The onset of the positive inotropic response to Rb+ or Tl+ was not dependent on the number of contractions which is in contrast to the cardiac glycoside-induced inotropic response. Substitution of 20 mM LiCl for an equimolar amount of NaCl in Krebs-Henseleit solution produced a significantly greater inotropic response than that observed when sucrose was substituted for NaCl. It appears that, among monovalent cations, only sodium pump inhibitors produce a sustained positive inotropic response.
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PMID:Effects of monovalent cations on cardiac Na+, K+-ATPase activity and on contractile force. 12 26

The temperature dependence of the transepithelial potential difference (PD) of the main duct of the submaxillary gland has been measured during in vitro perfusion studies. The magnitude of the PD depends strongly on the anion composition of the perfusing and bathing fluids. The following combinations of perfusion and bathing fluids respectively were used: (1) Na2SO4/NaCl, (2) Na2SO4, (3) NaCl/-NaCl, (4) NaCl/Na2SO4. The mean transepithelial potential differences at 35 degrees C with these four sets of conditions were respectively: 144, 148, 10 and - 15 mV, serosal side positive with respect to lumen. From the data obtained it was possible to construct Arrhenius plots of temperature dependence of the PD for the four sets of experimental conditions. They all show a breakpoint between 16 and 19 degrees C. The apparent activation energies in the four situations above the breakpoint are 4.2, 1.4, 12.0 and 10.6 kcal/mol, respectively. Below the breakpoint they are 29.9, 37.5, 29.0 and 31.3 kcal/mol, respectively. The rapid change in the PD as a function of temperature (which can also be achieved by the addition of ouabain), the effects of the removal of K+ on the serosal side on the PD, the decrease in the PD after the addition of ouabain or CN-, and the activation energies and breakpoints all lead to the conclusion that a large part of the PD is caused by an electrogenic sodium pump which is very probably the enzyme (Na+ plus K+)-ATPase. When the duct is perfused with Na2SO4 we find, above the breakpoint in the Arrhenius plots, a lower activation energy than is found when perfusing with NaCl.
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PMID:Evidence for electronogenic sodium pumping in the ductal epithelium of rabbit salivary gland and its relationship with (Na+ plus K+)-ATPase. 12 82

Ultrasonic treatment of microsome fraction or the preparation of partially purified Na+, K+-ATPase from cattle brain resulted in the formation of closed structures which immobilized rubidium and sodium ions and were easily discovered in electron microscope. Gradual release of bound rubidium ions was observed under the incubation of ultrasonic-treated membrane preparation in salt solutions. This process was activated by ATP. ATP-activated release of rubidium was observed only in the presence of sodium and was inhibited by ouabain. A hypothesis on the participation of sodium pump in the ion transport through membranes of artificial vesicles is discussed.
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PMID:[Properties of artificial vesicles from biological membranes]. 12 87

Relationships among positive inotropic responses, (Na+,K+)-ATPase inhibition, and sodium pump activities were studied using paced Langendorff preparations of guinea pig heart. (Na+,K+)-ATPase activity was estimated from the initial velocity of [3H] ouabain binding in ventricular homogenates, and sodium pump activity from ouabain-sensitive 86Rb uptake of ventricular slices. These parameters were measured in control, or in ouabain-or digitoxin-treated hearts either at the time of inotropic response or during the course of drug washout and compared with inotropy in the same heart. Perfusion of ouabain or digitoxin caused an increase in contractile force and a decrease in the initial velocity of ATP-dependent [3H] ouabain binding. The levels of [3H] ouabain binding in homogenates observed after a long incubation period were not different in ouabain-perfused and control homogenates, indicating that the nonlabeled ouabain bound to (Na+,K+)-ATPase during Langendorff perfusion was exchangeable with [3H] ouabain. Perfusion of drug-free solution after a 20-min perfusion of the isolated heart with either ouabain or digitoxin resulted in a loss of inotropic response and a recovery of the inhibition of the initial velocity of ATP-dependent [3H] ouabain binding. Inotropic responses to digitoxin during perfusion and subsequent loss during washout were accompanied by a reduction and subsequent recovery of ouabain-sensitive 86Rb uptake. Thus, it would appear that with cardiac glycosides, a relationship exists among cardiac contractile force, the inhibition of cardiac (Na+,K+)-ATPase, and the inhibition of the sodium pump activity. The inhibition of (Na+,K+)-ATPase and sodium pump because of cardiac glycoside perfusion of the isolated beating heart was reversible.
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PMID:Cardiac glycosides: relationship among active 86Rb uptake, (Na+,K+)-ATPase activity, and inotropy in guinea pig heart. 13 Jun 62

A significant mean increase of 18% in erythrocyte sodium pump activity (p less than 0.01, t test) was observed during lithium treatment, as compared with the activity before lithium treatment was started, in a group of 20 patients who were treated with lithium therapy for a variety of psychiatric conditions. The mean level of erythrocyte membrane ouabain-sensitive ATPase activity in a group of 35 subjects who were receiving lithium therapy was significantly higher than that of a different group of 38 subjects who were not receiving lithium therapy (p less than 0.005, t test). These observations may offer a biochemical mode of action for lithium in the treatment of bipolar affective disorder, since a deficiency of sodium pump activity has been shown to be associated with that disorder.
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PMID:Increased erythrocyte Na+ pump and NaK-ATPase activity during lithium therapy. 13 87

At [Na+]o = 118 mM the concentrative transfer of cholic and taurocholic acid from the perfusate into the isolated rat liver displays saturation kinetics (taurocholate: V = 299 nmol-min-1-g-1, Km = 61 muM; Cholate: V=327 nmol-min-1-g-1, Km = 436 muM). Perfusion with an isotonic sodium-free medium did not change the feature of a carrier-mediated transport but did markedly reduce V without affecting Km (taurocholate: V = 65 nmol-min-1-g-1, Km = 78 muM; cholate: V = 104 nmol-min-1-g-1, Km = 354 muM). It was experimentally assured that the observed reduction of bile salt uptake was not a consequence of regurgitation of bile salts or due to an excessive intracellular accumulation during cholestasis in the sodium-free state. The rate of taurocholate efflux is very low when compared with the rapid rate of the uptake. A stimulatory action of extracellular sodium on this pathway was also observed. Inhibition of the (Na+ + K+)-ATPase by 1 mM ouabain resulted in a decrease of bile salt uptake. Activation of the enzyme by potassium readmission to a K+-deprived liver enhanced bile salt uptake. The immediate response to alteration of the enzyme activity suggests a close association of a fraction of bile acid active transport with the sodium pump.
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PMID:Investigations on the sodium dependence of bile acid fluxes in the isolated perfused rat liver. 13 26

The relationship between altered transmembrane sodium movements and myocardial contractility was studied by opposing the action of the sodium pump with grayanotoxin I (GTX), an agent previously shown to increase resting sodium influx. GTX failed to affect Na+,K+-adenosine triphosphatase activity in vitro in concentrations as high as 0.1 mM. In electrically driven left atrial preparations of guinea-pig hearts, 1 mugM GTX produced a slight depolarization and appeared to decrease the upstroke velocity of the action potential, GTX (0.1-1 mugM) also produced a positive inotropic effect which developed over a 20-minute period. At higher concentrations, GTX produced arrhythmias. These effects of GTX were also observed in the presence of 10 mugM propranolol. Positive inotropic and arrhythmic effects of GTX were reversible after washout of the drug. These effects of GTX were also reversed by tetrodotoxin, an agent which has been shown to counteract the effect of GTX on sodium permeability. These data are consistent with a hypothesis that altered transmembrane sodium movement effects myocardial contractility.
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PMID:Effects of grayanotoxin I on cardiac Na + K + -adenosine triphosphatase activity, transmembrane potential and myocardial contractile force. 13 36


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