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)

In hyperthyroidism, erythrocytes show decreased Na+,K+-ATPase activity, decreased [3H]ouabain binding capacity (an index of the number of sodium pumps) and decreased active sodium and potassium flux rates, with a high intracellular sodium concentration. As erythrocytes are non-nucleated and atypical cells, we have studied electrolyte status in thyroid disease using mixed leucocytes as well; the results obtained differed from those in erythrocytes. When compared with findings in healthy subjects, leucocyte Na+,K+-ATPase activity, [3H]-ouabain binding capacity, total and active rubidium (used instead of potassium) influx were all significantly increased in untreated hyperthyroidism and decreased in untreated hypothyroidism. In hyperthyroidism, there was also a decrease in plasma potassium, an increase in sodium efflux rate and efflux rate constant, but no significant changes in cell sodium and potassium concentrations. All these changes returned to normal in successfully treated patients. There was a significant correlation between these abnormalities of electrolyte status and thyroid disease status (as serum thyroid stimulating hormone and free thyroxine).
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PMID:Ion flux and Na+,K+-ATPase activity of erythrocytes and leucocytes in thyroid disease. 302 98

Isolated hepatocytes from the elasmobranch Raja erinacea were examined for their regulatory responses to a solute load following electrogenic uptake of L-alanine. The transmembrane potential (Vm) was measured with glass microelectrodes filled with 0.5 M KCl (75 to 208 M omega in elasmobranch Ringer's solution) and averaged -61 +/- 16 mV (S.D.; n = 68). L-Alanine decreased (depolarized) Vm by 7 +/- 3 and 18 +/- 2 mV at concentrations of 1 and 10 mM, respectively. Vm did not repolarize to control values during the 5-10 min impalements, unless the amino acid was washed away from the hepatocytes. The depolarizing effect of L-alanine was dependent on external Na+, and was specific for the L-isomer of alanine, as D- and beta-alanine had no effect. Hepatocyte Vm also depolarized on addition of KCN or ouabain, or when external K+ was increased. Rates of 86Rb+ uptake and efflux were measured to assess the effects of L-alanine on Na+/K+-ATPase activity and K+ permeability, respectively. Greater than 80% of the 86Rb+ uptake was inhibited by 2 mM ouabain, or by substitution of choline+ for Na+ in the incubation media. L-Alanine (10 mM) increased 86Rb+ uptake by 18-49%, consistent with an increase in Na+/K+ pump activity, but had no effect on rubidium efflux. L-Alanine, at concentrations up to 20 mM, also had no measurable effect on cell volume as determined by 3H2O and [14C]inulin distribution. These results indicate that Na+-coupled uptake of L-alanine by skate hepatocytes is rheogenic, as previously observed in other cell systems. However, in contrast to mammalian hepatocytes, Vm does not repolarize for at least 10 min after the administration of L-alanine, and changes in cell volume and potassium permeability are also not observed.
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PMID:Effects of L-alanine on membrane potential, potassium (86Rb) permeability and cell volume in hepatocytes from Raja erinacea. 320 43

The stimulation of DNA synthesis by serum is accompanied by early (30 minutes) and late (2-8 hours) increase in ouabain-sensitive rubidium (potassium) influx and the elevation of intracellular potassium content from 0.5-0.6 to 0.7-0.8 mmole per gram protein in CHO-K1 cells. Isoproterenol alone induces the transient increase both in potassium influx via Na,K-ATPase and in potassium efflux without any effect on intracellular potassium content and cell proliferation. Isoproterenol acts synergistically with serum in eliciting the early and late changes in potassium transport and in stimulating G1----S transition. The combination of serum and theophylline produces a rapid increase in potassium influx, however, it does not stimulate DNA synthesis and does not induce any later increase in intracellular potassium content. It is concluded that early and late activation of Na,K-ATPase by mitogens can be dissociated; the Na,K-ATPase activation is involved in mitogenic response when producing the sustained potassium influx and the elevation of intracellular potassium content during G1----S transition.
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PMID:[Early and late changes in potassium transport during the start of proliferation in CHO cell cultures. The action of serum, isoproterenol, propranolol and theophylline]. 324 89

Urinary samples were collected from individuals not taking cardiac glycosides. Aliquots of 30 ml were passed through preparative octadecylsilane-bonded phase columns and eluted in fractions by stepwise increasing concentrations of acetonitrile. Eluted fractions were analysed for their contents of endogenous digoxinlike substance (EDLS) by radioimmunoassay of digoxin and by a bioassay of cardiac glycosides, which measures the uptake of rubidium (86Rb) by erythrocytes as an index of Na+, K+-ATPase activity. In both assays, digoxinlike activity was found in several fractions, but the highest values were consistently measured in the fractions eluted with 40% acetonitrile. Greater amounts of EDLS were recovered from the urine of pregnant women than from the urine of men and nonpregnant women.
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PMID:Partial characterization of endogenous digoxinlike substance in human urine. 328 7

In order to assess the effects of glucose, insulin, and exercise on skeletal muscle blood flow in vivo, we measured positron emission from the thigh muscle of anesthetized rabbits after simultaneous aortic bolus injection of 82Rb and radiolabeled microspheres (15 micron diameter). Estimates of flow with 82Rb were based on first-pass regional extraction of 82Rb by skeletal muscle. Flow estimates were made serially as a function of variations in plasma glucose and insulin and changing the muscle contractile state by electrical stimulation. Flow ranged from 3.1 ml/min/100 g at rest to 71 ml/min/100 g during stimulation. There was good agreement between the two methods of flow measurement over the entire range of flows (r = 0.96 at a slope of 0.90). Flow measured by either method did not vary significantly from baseline over a range of plasma glucose from 5 to 30 mM and plasma insulin from 0 to 20 microU/ml. When flow was increased up to 20-fold by electrical stimulation there was a decrease in extraction of 82Rb proportional to the increase in flow. However, at pharmacologic levels of insulin (greater than 150 microU/ml) flow was increased twofold as measured by radiolabeled microspheres, but not as measured by rubidium. There was no apparent decrease in extraction of 82Rb with high insulin. The discrepancy between the microsphere measured flow and rubidium measured flow with high plasma insulin levels can be explained by the assumption that the expected decrease in the extraction fraction was counteracted by an increase in Na+/K+-ATPase activity. It is concluded that the first-pass flow model gives valid estimates of skeletal muscle blood flow in vivo with 82Rb, provided that plasma insulin levels are normal.
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PMID:Skeletal muscle blood flow in vivo: detection with rubidium-82 and effects of glucose, insulin, and exercise. 329 72

In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations after the oral administration of rubidium chloride. In this paper we describe our findings in 22 patients with untreated essential hypertension, compared with the findings in 22 carefully matched control subjects. Our findings in patients receiving short-term digoxin therapy and in patients with chronic renal failure are also included for comparison. Whereas the findings in patients receiving digoxin and in patients with chronic renal failure are compatible with a widespread reduction in sodium, potassium-ATPase activity in vivo, the findings in patients with untreated essential hypertension are not. Further analysis of the data and a similar study of the disposition of 42K after the intravenous administration of 42KCl suggest that in vivo net cation transport is enhanced in the erythrocytes of patients with untreated essential hypertension.
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PMID:Cation transport abnormalities in vivo in untreated essential hypertension. 370 67

Na-K-Cl cotransport stoichiometry and affinities for Na, K and Cl were determined in flounder intestine. Measurement of simultaneous NaCl and RbCl influxes resulted in ratios of 2.2 for Cl/Na and 1.8 for Cl/Rb. The effect of Na and Rb on Rb influx showed first order kinetics with K1/2 values of 5 and 4.5 mM and Hill coefficients of 0.9 and 1.2, respectively. The effect of Cl on rubidium influx showed a sigmoidal relationship with K1/2 of 20 mM and a Hill coefficient of 2.0. The effects of variations in Na and Cl concentration on short-circuit current (Isc) were also determined. The K1/2 for Na was 7 mM with a Hill coefficient of 0.9 and the K1/2 for Cl was 46 mM with a Hill coefficient of 1.9. Based on the simultaneous influx measurements, a cotransport stoichiometry of 1Na:1K:2Cl is concluded. The Hill coefficients for Cl suggest a high degree of cooperativity between Cl binding sites. Measurements of the ratio of net Na and Cl transepithelial fluxes under short-circuit conditions (using a low Na Ringer solution to minimize the passive Na flux) indicate that the Cl/Na flux ratio is approximately 2:1. Therefore, Na recycling from serosa to mucosa does not significantly contribute to the Isc. Addition of serosal ouabain (100 microM) inhibited Rb influx, indicating that Na-K-Cl cotransport is inhibited by ouabain. This finding suggests that a feedback mechanism exists between the Na-K-ATPase on the basolateral membrane and the apical Na-K-2Cl cotransporter.
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PMID:Stoichiometry and ion affinities of the Na-K-Cl cotransport system in the intestine of the winter flounder (Pseudopleuronectes americanus). 373 4

The causes of central nervous system (CNS) dysfunction in uremia are not well known and are not completely reversed by dialysis. This problem was investigated in synaptosomes, which are membrane vesicles from synaptic junctions in the brain. We measured Na uptake under conditions of control, veratridine stimulation, and tetrodotoxin inhibition, in synaptosomes from normal and acutely uremic (blood urea nitrogen, 250 mg/dl) rats. In the control state, maximal Na uptake was 2.2 +/- 0.2 and 1.9 +/- 0.3 nmol/mg of protein in normal and uremic synaptosomes, respectively. With veratridine stimulation, Na uptake was increased by 1.9 and 3.6 nmol/mg of protein in normal vs. uremic rats (P less than 0.001). The increased veratridine-stimulated Na uptake observed in uremia could be due either to increased membrane permeability to Na or decrease in the Na-K ATPase pump activity. To investigate this, we studied the Na-K ATPase pump function by evaluating uptake of K (using rubidium as a tracer), uptake of Na during ATP stimulation, and inhibition of Rb and Na uptake by ouabain. In uremic rats both Rb uptake and ATP-stimulated Na uptake were significantly less than in normals (P less than 0.005). This suggests a defect in the Na-K ATPase pump. Membrane permeability for Na was then evaluated both by measuring initial Na uptake, and with addition of valinomycin. No change in Na uptake pattern was observed with valinomycin, and initial Na uptake was not significantly different in normal versus uremic synaptosomes. These data show that (a) in uremic rats veratridine-stimulated Na accumulation is significantly greater than normal; (b) the increased Na accumulation observed in uremia appears to be due to alterations in Na-K ATPase pump activity; and (c) the altered Na accumulation observed is probably not due to a uremic environment, but may be secondary to a physiologic alteration in synaptosomal function due to the uremic state. These abnormalities may affect neurotransmission and may be associated with the CNS alterations observed in uremia.
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PMID:Abnormal sodium transport in synaptosomes from brain of uremic rats. 400 50

1. The secretion of sodium, potassium and lithium has been studied in the isolated cat pancreas, perfused with bicarbonate buffered saline solutions of varying composition and osmolality, and stimulated maximally with secretin.2. Under isosmolal conditions, when perfusate sodium chloride was replaced by sucrose, sodium secretion and potassium secretion were directly related to perfusate sodium concentration, [Na](p).3. When osmolality was varied by increasing or decreasing perfusate sodium chloride concentration, the secretion of sodium and of potassium were maximal at [Na](p) of about 120 and 80 mM respectively.4. At a given [Na](p), sodium secretion was greater under hypo-osmolal conditions than under isosmolal conditions.5. When potassium concentration was varied over the range 0-130 mM under isosmolal conditions, by adjusting perfusate NaCl concentration, the secretion of potassium and of sodium were maximal at [K](p) of about 50 and 10 mM respectively. Water flux was maximal at a [K](p) of 10-15 mM. The concentration of potassium in the secretion was almost identical with that in the perfusate over the whole concentration range.6. Replacement of perfusate sodium by lithium reduced the volume of secretion, though a small secretion was maintained even in the complete absence of sodium. The concentration of lithium in the secretion was generally slightly greater than that in the perfusate.7. Omission of potassium from the perfusate reduced secretion by about 65%. Rubidium was a complete substitute for potassium; caesium was not.8. Energy for secretion is derived largely from oxidative phosphorylation. Secretion was reduced by more than 90% under anaerobic conditions and in the presence of dinitrophenol or cyanide. Removal of glucose from the perfusate reduced secretion by more than 50% within 30 min; lactate was a complete substitute for glucose.9. Ouabain, ethacrinic acid and frusimide, known inhibitors of Na(+), K(+)-ATPase activity, all inhibited pancreatic electrolyte secretion.10. The observations are interpreted with reference to the nature of active transport processes involved in pancreatic electrolyte secretion.
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PMID:The secretion of alkali metal ions by the perfused cat pancreas as influenced by the composition and osmolality of the external environment and by inhibitors of metabolism and Na+, K+-ATPase activity. 428 36

Ethynylestradiol impairs bile flow and bile salt maximum secretory rate in rats, implying a secretory defect. In addition, Na-K-ATPase activity is decreased in liver surface membranes, suggesting abnormalities at the sinusoidal as well as the canalicular membrane. We investigated whether ethynylestradiol pretreatment affects bile salt uptake and Na-K pump function in isolated rat hepatocytes. Ethynylestradiol-treated cells were functionally intact as assayed with trypan blue exclusion, lactate dehydrogenase release, and oxygen consumption. Initial taurocholate uptake velocity was reduced by 73% in ethynylestradiol-treated hepatocytes [Vmax, 1.0 +/- 0.1 vs. 3.7 +/- 0.2 mumol X min-1 X (10(6) cells)-1; P less than 0.001; Km, 34 +/- 5 vs. 33 +/- 3 microM]. Na-K-ATPase activity in cell homogenates (36 +/- 5 vs. 27 +/- 4 mumol Pi X h-1 X mg prot-1; P less than 0.05), ouabain-suppressible rubidium-86 influx [6.8 +/- 1.1 vs. 4.8 +/- 1.0 nmol K+ X min-1 X (10(6) cells)-1; P less than 0.05], and intracellular potassium concentration (126 +/- 10 vs. 110 +/- 16 mmol/l; P less than 0.05) were reduced after ethynylestradiol. Taurocholate uptake measured at different temperatures between 25 degrees and 37 degrees was linear when plotted according to Arrhenius. The energy of activation was increased by 40% in ethynylestradiol-treated hepatocytes [17 +/- 4 vs. 23 +/- 4 kcal X mol-1 X (10(6) cells)-1; P less than 0.05], consistent with decreased membrane fluidity. These data suggest the possibility that during ethynylestradiol-induced cholestasis a disorder of the sinusoidal domain, caused perhaps by ethynylestradiol-induced alterations in membrane lipid composition, is an important contributing factor.
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PMID:Ethynylestradiol impairs bile salt uptake and Na-K pump function of rat hepatocytes. 609 53


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