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)

1. The effects of prostaglandin E2 (PGE2) on ion transport were investigated in guinea-pig isolated gastric mucosa. 2. Under resting conditions the mucosa produced a short-circuit current (SCC), the majority of which could be attributed to electrogenic chloride secretion. This interpretation was confirmed by the dependence of the basal SCC on extracellular chloride, and inhibition by the chloride channel blocker, diphenylamine-2-carboxylate. The mucosa also exhibited low rates of acid secretion and of sodium and rubidium absorption. 3. PGE2 stimulated an increase in net chloride secretion which was more than sufficient to account for the concomitant increase in SCC. As with the basal SCC, the SCC response to PGE2 was chloride dependent and inhibited by diphenylamine-2-carboxylate. PGE2 also significantly increased acid secretion and net rubidium absorption, but these changes were not sufficient to account for SCC. 4. The H+-K+-ATPase inhibitor, omeprazole, inhibited basal and PGE2-stimulated acid secretion, but did not modify the effects the PGE2 on net chloride secretion, SCC or conductance, suggesting that these effects of PGE2 were not related to changes in gastric acid secretion. 5. Both basal and PGE2-stimulated SCC were dependent on extracellular sodium and inhibited by ouabain, indicating the importance of a sodium gradient and the Na+-K+-ATPase in maintaining the electrogenic properties of the mucosa. 6. These results are consistent with the view that PGE2 stimulates electrogenic chloride secretion in guinea-pig gastric mucosa, and provide an ionic basis for the stimulation of secretion of sodium and chloride by prostaglandins observed in mammalian gastric mucosa in vivo.
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PMID:Stimulation of electrogenic chloride secretion by prostaglandin E2 in guinea-pig isolated gastric mucosa. 245 57

Dysprosium(III) triethylenetraamine-N,N,N',N",N"',N"'-hexaacetic acid (DyTTHA3-) was used as an aqueous chemical shift reagent in conjunction with high-resolution nuclear magnetic resonance (NMR) spectroscopy to monitor 87-rubidium (87Rb+) transport in human erythrocyte suspensions. NMR spectra demonstrated two resonances which were assigned to the intra- and extracellular compartments of the erythrocyte suspension. Uptake of 87Rb+ was shown to proceed via the [Na,K]-ATPase dependent pump as evidenced by the inhibition of uptake in the presence of ouabain. The steady state intra- to extracellular concentration ratio of 87Rb was 3.00 and 1.13 in the absence and presence of ouabain, respectively. The rate of uptake of 87Rb+ in the absence and presence of ouabain was found to be 1.3 and 0.5 mmol Rb+/L erythrocytes/h at 18 mM Rb+, respectively. Data are also presented which indicate that the intracellular component of 87Rb is less than 100% NMR visible.
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PMID:Rubidium transport in human erythrocyte suspensions monitored by 87Rb NMR with aqueous chemical shift reagents. 251 54

The expression of Na+-K+ ATPase pumps was studied in cultured human retinal pigment epithelium (RPE). Pump site number was measured by quantitation of the specific binding of [3H]ouabain to cultures of varying density. Specific binding of [3H]ouabain was time- and concentration-dependent, and was inhibited by potassium and by excess unlabeled ouabain. Estimates of pump site number based upon specific [3H]ouabain binding indicated that the number of pumps per RPE cell was maximal in sparse cultures and declined six-fold as cultures became confluent. Pump activity, determined by measurement of specific 86Rb (rubidium) uptake, was also greater in sparse than in dense cultures. Quantitation of [3H]thymidine incorporation as a measure of cell proliferation demonstrated that proliferation in RPE cultures decreased logarithmically as culture density increased. Increased pump site number in cultured RPE, therefore, correlated with increased cell proliferation and decreased culture density. We conclude that human RPE express ouabain-sensitive Na+-K+ ATPase in vitro and maximal expression is observed in sparse, proliferating cultures.
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PMID:Ouabain-sensitive Na+-K+ ATPase pumps in cultured human retinal pigment epithelium. 253 43

We have developed and used a novel technique to investigate the effects of lithium and other psychotropic drugs on the cation-transporting properties of the sodium- and potassium-activated ATPase enzyme (Na+,K+-ATPase) in intact synaptosomes. Rubidium-86 uptake into intact synaptosomes is an active process and is inhibited by approximately 75% in the presence of the Na+,K+-ATPase inhibitor acetylstrophanthidin. In vitro addition of lithium to synaptosomes prepared from untreated mice causes a progressive inhibition of acetylstrophanthidin-sensitive 86Rb uptake, but only at concentrations higher than the clinical therapeutic range. However, pretreatment of mice for 14 days in vivo with lithium, carbamazepine, and haloperidol, but not phenytoin, causes a significant stimulation of 86Rb uptake into synaptosomes via Na+,K+-ATPase.
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PMID:Effect of lithium and of other drugs used in the treatment of manic illness on the cation-transporting properties of Na+,K+-ATPase in mouse brain synaptosomes. 253 59

1. We have measured cation transport in vivo in seven healthy volunteers under control conditions and after they had taken lithium carbonate for 21 days in doses which maintained the serum lithium concentration in the range 0.6-0.8 mmol/l. 2. We have measured cation transport in vivo after the administration of an oral load of rubidium chloride, and have found that, although intra-erythrocytic concentrations of rubidium were significantly lower 1 h after the administration of rubidium when the subjects were taking lithium, there was a significant increase in the rate of uptake of rubidium into the erythrocytes over the subsequent period of the test, suggesting a direct stimulation of sodium, potassium-activated adenosine triphosphatase by lithium. 3. Lithium administration did not affect the plasma concentration versus time profile of rubidium after the rubidium load, implying that the lithium-stimulated uptake of rubidium which occurs in erythrocytes does not necessarily occur in other cell types. 4. These results suggest that previous studies of cation transport using peripheral cells and assay systems in vitro do not necessarily reflect changes in cation transport in vivo in excitable tissues.
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PMID:Measurement of cation transport in vivo in healthy volunteers after the oral administration of lithium carbonate. 254 Sep 32

The (Na+ + K+)-ATPase (sodium pump) is an ouabain-sensitive, electrogenic ion pump responsible for maintaining the balance of sodium and potassium ions in almost all animal cells. Robust, ouabain-sensitive rubidium uptake, indicative of the sodium pump, was found in tissue-cultured Drosophila cells, and both larvae and adults die when fed a diet containing ouabain. A monoclonal antibody to the avian sodium pump alpha-subunit was found to cross-react with the Drosophila sodium pump alpha-subunit. Immunofluorescence microscopy was used to obtain a semi-quantitative view of the expression of the sodium pump in Drosophila tissues: high levels of the sodium pump were detected in malpighian tubules, indirect flight muscles and tubular muscles, and throughout the nervous system. The cDNA encoding this sodium pump alpha-subunit in Drosophila melanogaster was cloned, sequenced and expressed in mouse L cells. At the amino acid level, its deduced sequence of 1038 residues (the first such sequence for an invertebrate) is approximately 80% similar to alpha-subunit sequences reported for vertebrates. Only one gene was found in Drosophila, located on the third chromosome at position 93B. A restriction site polymorphism has been found, and several mutations exist that may involve the alpha-subunit gene.
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PMID:Molecular characterization and expression of the (Na+ + K+)-ATPase alpha-subunit in Drosophila melanogaster. 254 Sep 56

The ability of plasma to inhibit 86 rubidium uptake in rat aorta and to displace [3H]-ouabain from hog brain Na+,K+-ATPase was used as a measure of plasma Na+,K+-ATPase inhibitory activity in seven normotensive and eight hypertensive subjects. Rat aortae rings were incubated in oxygenated plasma containing 86 rubidium (2 microCi/mL) for 30 mins at 37 degrees C and uptake measured and expressed as mumol/kg wet weight/min. Plasma was extracted with a mixture of chloroform and methanol (2:1) and the extract separated by silicic acid column followed by thin layer chromatography and fractions assayed for ouabain displacement using digoxin as a standard. Total ouabain displacement was calculated as the sum of all fractions. There was a strong correlation between the two methods for total plasma Na+,K+-ATPase inhibitory activity (r = 0.761, P less than 0.01). There was a significant positive correlation between plasma Na+,K+-ATPase inhibitory activity and blood pressure in all subjects. Na+,K+-ATPase inhibitory activity was significantly higher in plasma of hypertensives by both methods (P less than 0.001). The increased Na+,K+-ATPase inhibitory activity in plasma from hypertensives was due to the nonesterified fatty acid, long chain acylcarnitine and diphosphatidylglycerol fractions.
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PMID:Higher plasma Na+,K+-ATPase inhibitory activity in essential hypertensive patients. 254 1

Although active transport of potassium into human platelets has been demonstrated previously, there is hitherto no evidence that human platelets have an ouabain-inhibitable Na-K ATPase in their membrane. The present study demonstrates active rubidium (used as an index of potassium influx), 86Rb(K), influx into platelets, inhibitable by ouabain, and also demonstrates the presence of specific [3H]ouabain binding by the human platelet. This 86Rb(K) influx was stimulated by adrenaline, isoprenaline, and salbutamol, but noradrenaline caused a mild inhibition. Active 86Rb(K) influx by platelets was inhibited markedly by timolol, mildly by atenolol, but not by phentolamine. Therefore, active 86Rb(K) influx in human platelets is enhanced by stimulation of beta adrenoceptors of the beta 2 subtype. The platelet may therefore replace the leukocyte in future studies of Na-K ATPase activity. This would be a considerable advantage in view of the ease and rapidity of preparation of platelets.
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PMID:86Rb(K) influx and [3H]ouabain binding by human platelets: evidence for beta-adrenergic stimulation of Na-K ATPase activity. 254 65

1. When magnesium and orthophosphate are added to Na+,K+-ATPase containing occluded rubidium ions, and suspended in a medium containing free rubidium ions, only 50% of the occluded rubidium is released rapidly. This is because the release of occluded rubidium is ordered, and the replacement (by rubidium ions from the medium) of the first occluded rubidium ions to leave slows the departure of the remaining occluded ions. 2. Since the Na+,K+-ATPase probably exists in the membrane as a structural dimer, the ordered release might represent either the ordered emptying of the two halves of the dimer, or the ordered release of the two rubidium ions thought to be contained in each promoter. 3. The present experiments were designed to decide between these possibilities by examining the behaviour of Na+,K+-ATPase in which about half of the protomers had been randomly inactivated by pre-treatment either with fluorescein isothiocyanate or with alpha-chymotrypsin. 4. The results show that the release of rubidium ions from each protomer is ordered.
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PMID:Evidence for the ordered release of rubidium ions occluded within individual protomers of dog kidney Na+,K+-ATPase. 255 Jun 27

The number and activity of erythrocyte ATPase-dependent sodium-potassium pump units were increased in obese subjects (p = 0.02). No link was observed between the number or activity of the pump units and hypertension. The ouabain-insensitive rubidium (i.e. potassium) transport was not associated with relative body weight or blood pressure status. Sodium-lithium countertransport correlated significantly with obesity but not with blood pressure status. In the hypertensive patients, before or after therapy with verapamil, hydrochlorothiazide, pindolol or atenolol there were no significant differences in cation transport. We propose that the correlation between obesity and essential hypertension cannot be explained by these two cation transport systems.
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PMID:Erythrocyte cation transport in obesity, hypertension, and during antihypertensive drug therapy. 257 70


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