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)

Net hepatic Ca2+ efflux, K+ uptake and glycogen breakdown in response to the alpha 1-adrenergic agonist phenylephrine were studied. Rat livers were perfused with CO2/bicarbonate-buffered solutions containing 10 microM Ca2+ and different amounts of Mg2+. K+-free medium and/or ouabain were used to block (Na+ + K+)-ATPase-dependent K+ uptake. In some experiments a sharp increase in extracellular Ca2+ concentrations was produced by infusing CaCl2 into the medium entering the liver. Perfusion with K+-free medium and ouabain enhanced the phenylephrine-induced Ca2+ efflux and diminished the glycogenolytic response, indicating a dissociation of Ca2+ release and glycogenolysis. Exogenous Ca2+ had practically no effect if livers were perfused with regular medium containing 1.2 mM Mg2+. In the presence of phenylephrine and if extracellular Mg2+ concentrations were lowered by omitting Mg2+ from the medium or by preperfusion with EGTA, exogenous Ca2+ was glycogenolytically effective and also produced a transient K+ uptake. Increased extracellular concentrations of Mg2+ inhibited the effects of exogenous Ca2+. In the presence of phenylephrine, higher concentrations of Mg2+ were needed than in the absence of alpha 1-adrenergic agonist to achieve a similar degree of inhibition. In one respect ouabain effects were comparable to those of phenylephrine: the glycoside also increased the metabolic response to exogenous Ca2+ and diminished the sensitivity towards Mg2+. Phenylephrine and ouabain may both enhance the permeability of plasma membranes for Ca2+.
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PMID:The hepatic response to Ca2+ is inhibited by Mg2+ and enhanced by phenylephrine or ouabain. 391 85

1. A study was made of the dependence on external Na of the movements of Na and K in human red cells. Special attention was given to ouabain-insensitive movements. The effect of internal Na on Na influx, and the influence of some sulphydryl inhibitors on ion movements and metabolism was also investigated.2. External Na stimulated ouabain-insensitive Na efflux and K influx. There was also a ouabain-insensitive component of Na influx that was raised on increasing the internal Na concentration. Exchange diffusion of Na appears to occur in the presence of ouabain and external K.3. Net transport of Na and K in the presence of ouabain was independent of external Na, as was also lactate production.4. Ethacrynic acid partially inhibited the Na pump; the Na-dependent components of Na efflux and K influx in the presence of ouabain were completely inhibited by ethacrynic acid. Both ouabain-sensitive and ouabain-insensitive adenosinetriphosphatase activities were inhibited by ethacrynic acid indicating a non-specific effect of this compound. Iodoacetamide decreased only the ouabain-insensitive ATPase activity.5. The results suggest that when the Na pump is blocked by ouabain, part of the residual ion movements can be attributed to exchange diffusion.
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PMID:Ion movements in human red cells independent of the sodium pump. 423 87

Total ischaemia of loops of dog colon was induced by clamping all afferent arteries and the colonic wall for different periods of time.Net sodium transport across the mucosa is abolished after one hour's ischaemia, but Na(+)-K(+)-ATPase levels in microsomal suspensions from the mucosa only fall significantly after two hours' ischaemia. Studies on the functional and morphological recovery of colons subjected to three hours' ischaemia have disclosed an extremely heterogeneous response among the 24 dogs used. Although all parameters were non-existent 24 hours after the intervention, one colon revealed a morphological and functional recovery one week after the operation, whilst two, three, and three out of six recovered after two, three, and four weeks respectively. There was a good correlation between the functional and macroscopic appearance of these recovered loops, though histologically various degrees of disorganization of the mucosa were observed. Among the loops that had no function, there was also a considerable variation in their microscopic structures. The level of Na(+)-K(+)-ATPase in the mucosa was found to be a faithful indicator of the functional state of the tissue, and could be closely correlated with the morphological findings.
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PMID:Functional and morphological response of the dog colon to ischaemia. 426 58

1. Acute NH(4) (+) toxicity was studied by using a new apparatus that removes and freezes the brains of conscious rats within 1s. 2. Brains were removed and frozen 5min after intraperitoneal injection of ammonium acetate (2-3min before the onset of convulsions). Arterial [NH(4) (+)] rose from less than 0.01 to 1.74mm at 4-5min. The concentrations of all glycolytic intermediates measured, except glucose 6-phosphate, were increased by the indicated percentage above the control value as follows: glucose (by 41%), fructose 1,6-diphosphate (by 133%), dihydroxyacetone phosphate (by 164%), alpha-glycerophosphate (by 45%), phosphoenolpyruvate (by 67%) and pyruvate (by 26%). 4. Citrate and alpha-oxoglutarate concentrations were unchanged and that of malate was increased (by 17%). 5. Adenine nucleotides and P(i) concentrations were unchanged but the concentration of creatine phosphate decreased slightly (by 6%). 6. Brain [NH(4) (+)] increased from 0.2 to 1.53mm. Net glutamine synthesis occurred at an average rate of 0.33mumol/min per g. 7. The rate of brain glucose utilization was measured in vivo as 0.62mumol/min per g in controls and 0.81mumol/min per g after NH(4) (+) injection. 8. The arteriovenous difference of glucose and O(2) increased by 35%. 9. No significant arteriovenous differences of glutamate or glutamine were detected. Thus, although much NH(4) (+) was incorporated into glutamine the latter was not rapidly released from the brain to the circulation. 10. Plasma [K(+)] increased from 3.3 to 5.4mm. 11. The results indicate that NH(4) (+) stimulates oxidative metabolism but does not interfere with brain energy balance. The increased rate of oxidative metabolism could not be accounted for only on the basis of glutamine synthesis. We suggest that increased extracellular [NH(4) (+)] and [K(+)] decreased the resting transmembrane potential and stimulated Na(+),K(+)-stimulated adenosine triphosphatase activity thus accounting for the increased metabolic rate.
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PMID:The acute action of ammonia on rat brain metabolism in vivo. 476 48

1. Spleen slices pre-incubated for different periods at 4 degrees C in Krebs solution containing varying concentrations of calcium, up to 96 mM, lost their endogenous noradrenaline stores when reincubated in normal Krebs solution at 37 degrees C for 2 hr. Rate of loss of noradrenaline was roughly related to the calcium concentration of the pre-incubation medium and the pre-exposure time.2. Pre-treatment with isotonic barium or strontium (96 mM) Krebs solution also induced release of noradrenaline from spleen slices when re-exposed to normal Krebs solution. Barium was more effective than either calcium or strontium.3. The enhanced release induced by calcium pre-treatment occurred in the absence of calcium, with or without EGTA.4. Tissue calcium concentration of spleen slices was 0.68 m-mole/kg. Pre-treatment of slices with normal or 96 mM calcium-Krebs solution for 4 hr at 4 degrees C increased the calcium concentration to 2.57 and 9.9 m-mole/kg, respectively.5. Ouabain, which caused a dose-dependent release of noradrenaline, did not modify the release induced by calcium pre-treatment.6. Spleen slices prepared from cats anaesthetized with sodium pentobarbitone instead of ether were resistant to noradrenaline depletion by calcium pre-treatment.7. Evoked release of [(3)H]noradrenaline by high potassium from calcium-pre-treated slices did not occur in the absence of external calcium, even though the calcium pre-treatment enhanced the tissue concentration of this ion by nearly tenfold.8. Net uptake of noradrenaline in normal and in treated slices whose noradrenaline content was severely reduced by barium pre-treatment or sodium withdrawal was comparable.9. Specific activity of released and endogenous [(3)H]noradrenaline increased as the tissue stores of noradrenaline were reduced.10. It is suggested that the spontaneous loss of tissue noradrenaline after pre-treatment with high-calcium solution was due to inhibition of sodium-potassium-activated ATPase by intracellular accumulation of calcium ions. Evidence is presented to suggest that vesicles depleted of their endogenous transmitter by pre-treatment with calcium, strontium or barium, or by sodium withdrawal, are re-used for the storage and release of exogenous noradrenaline.
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PMID:Release of noradrenaline from slices of cat spleen by pre-treatment with calcium, strontium and barium. 477 3

Net K+ fluxes in isolated hamster brown fat cells were studied by the use of the K+ analogue 86Rb+. In isolated cells, cold-stored overnight to diminish K+ gradients, an equilibrium 86Rb+ (K+) clearance value of 27 microliter/million cells was obtained after 30 min incubation at 37 degrees C. This corresponds to a 10-fold K+ gradient over the plasma membrane, and a K+ potential of about -60 mV. The attainment of this equilibrium was dependent upon the presence of Na+ in the extracellular medium, and the uptake was fully inhibited by the (Na+ + K+)-ATPase inhibitor ouabain. Ouabain had, however, no significant acute effect on the maximal rate of thermogenesis achieved after norepinephrine stimulation of the cells, but if the restoration of ionic equilibrium was inhibited by ouabain in prolonged incubations, a decreased thermogenesis was observed. This was probably due to the low cytosolic K+ content then encountered, and the resulting inhibition of lipolysis. The addition of norepinephrine to cells in which 86Rb+ (K+) equilibrium had been attained resulted in a rapid efflux of 86Rb+ and the establishment of a new equilibrium value, at about 65% of the unstimulated value. This corresponds to a decrease in K+ potential of about 15 mV. The effect of norepinephrine was stereospecific and reversible, and had an EC50 value of about 10 nM. As catecholamine effects were much more sensitive to phentolamine than to propranolol, the adrenergically-induced efflux was classified as predominantly alpha-adrenergic. It is suggested that the norepinephrine-induced K+ efflux is due to a (probably Ca2+-mediated) opening of K+ channels in the cell membrane, and that this effect occurs secondarily to the alpha-adrenergically induced membrane depolarization (and increase in cytosolic Ca2+). The increased PK over the cell membrane would counteract further depolarization, and the K+ gradient would then approach the Nernst equilibrium under the new steady-state conditions.
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PMID:Alpha-adrenergic effects on 86Rb+ (K+) potentials and fluxes in brown fat cells. 614 51

The F0F1-ATPase of the inner mitochondrial membrane catalyzes the conversion of a proton electrochemical energy into the chemical bond energy of ATP (Boyer, P.D., Chance, B., Ernster, L., Mitchell, P., Racker, E., and Slater, E.C. (1977) Annu. Rev. Biochem. 46, 955-1026). To assess the role of the membrane potential (delta psi) in this process and to study the effect of very short pulses on ATP synthesis, we employed a high voltage pulsation method (Kinosita, K., and Tsong, T.Y. (1977) Proc. Natl. Acad. Sci. U.S.A. 74, 1923-1927) to induce a delta psi of controlled magnitude and duration in a suspension of submitochondrial particles and F0F1-ATPase vesicles. Cyanide-treated submitochondrial particles were exposed to electric pulses of 10-30 kV/cm of magnitude (generating a peak delta psi of 150-450 mV) and 1-100 microseconds duration. Net [32P]ATP synthesis from [32P]Pi and ADP was observed with maximal values of 410 pmol/mg X pulse for a 30 kV/cm-100-microseconds pulse. This corresponds to a yield of 10-12 mol of ATP per mol of F0F1 complex per pulse. As many as 4 nmol/mg were produced after pulsing the same sample 8 times. By varying the ionic strength of the suspending medium, and consequently the pulse width, it is clearly shown that the synthesis was electrically driven and did not correlate with Joule heating of the sample. Titrations using specific inhibitors and ionophores were performed. The voltage-induced ATP synthesis was 50% inhibited by 0.11 microgram/mg of oligomycin and 2.4 nmol/mg of N,N'-dicyclohexylcarbodiimide. Ionophores and uncouplers had varying degrees of inhibition. The dependence of ATP synthesis on pulse width was nonlinear, exhibiting a threshold at 10 microseconds and a biphasic behavior above this value. Isolated F0F1-ATPase reconstituted into asolectin vesicles also synthesized ATP when pulsed with electric fields. A 35 kV/cm pulse induced the synthesis of 115 pmol of ATP per mg of protein, which corresponds to approximately 0.34 mol of ATP per mol of F0F1-ATPase. This synthesis was also sensitive to oligomycin and dicyclohexylcarbodiimide. The possibility of turnover of the ATPase in microseconds is considered.
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PMID:Voltage-driven ATP synthesis by beef heart mitochondrial F0F1-ATPase. 623 68

1. Phospholipid vesicles reconstituted with Na-K-ATPase from pig kidney, show slow passive pump-mediated (86)Rb fluxes in the complete absence of ATP and phosphate.2. The Rb fluxes are inhibited in vesicles prepared from enzyme pre-treated with either ouabain or vanadate ions. Rb fluxes through Na-K pumps oriented inside-out or right-side out by comparison with the normal cellular orientation can be distinguished by effects of vanadate on one or both sides of the vesicle.3. (86)Rb uptake into Rb-loaded vesicles represents a (86)Rb-Rb exchange. The maximal rate of exchange through inside-out and right-side out oriented pumps is equal, suggesting a random arrangement of the pumps across the vesicle membrane. This Rb-Rb exchange is half-saturated on inside-out and right-side out pumps at about 0.6 and 0.2 mM-external Rb respectively.4. (86)Rb uptake into Rb-free vesicles represents a net Rb flux. The Rb uptake through inside-out pumps has a maximal rate about equal to the Rb-Rb exchange, half-saturates at an external Rb concentration of roughly 0.5 mM, and shows evidence for co-operativity. Net Rb uptake through right-side out pumps is very slow, and half-saturates at roughly 0.1 mM external Rb.5. K ions at low concentrations in the exterior medium stimulate (86)Rb uptake, but at high concentrations, inhibit. Na ions in the exterior medium always inhibit (86)Rb uptake. The result suggests that K ions are transported in co-operative fashion together with Rb ions, while Na ions block the Rb fluxes.6. The presence of Rb congeners at the vesicle interior raises the (86)Rb uptake through inside-out pumps with the decreasing order of effectiveness: Li > Na > Cs > K > Rb. Stimulation by Na ions involves a Rb-Na exchange.7. Turnover numbers were estimated from parallel measurement of Na/K pump mediated fluxes and amount of covalent phosphoenzyme. In units of moles of ion per mole of phosphoenzyme per second at 20 degrees C the following values were obtained: ATP-dependent Na-Rb exchange, 43; (ATP+phosphate)-stimulated Rb-Rb exchange, 7. For (ATP+phosphate)-independent fluxes: Rb-Rb exchange 0.25; net Rb uptake 0.15 and Rb-Na exchange 0.65.8. Mg ions in the exterior medium inhibited both net and exchange Rb fluxes through inside-out pumps in a manner antagonistic with respect to Rb. Mg and vanadate ions inhibit the Rb fluxes in a synergistic fashion.9. The results are interpreted in terms of a model in which net and exchange (86)Rb fluxes occur via conformational transitions between form E(1) which binds Rb at the cytoplasmic face of the protein, the form E(2) (Rb)(occ) containing occluded Rb ions and a form E(2) which binds Rb at the extracellular face of the protein. A kinetic analysis allows us to identify rate-limiting steps of the transport cycle by making use of our transport data in combination with values of rate-constants for conformational transitions observed directly in isolated Na-K-ATPase.
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PMID:Passive rubidium fluxes mediated by Na-K-ATPase reconstituted into phospholipid vesicles when ATP- and phosphate-free. 629 Jun 46

Various parameters of erythrocyte membrane sodium transport were measured in patients with untreated essential hypertension, in the normotensive offspring of parents with hypertension, and in patients whose hypertension had been controlled by medication. Net sodium efflux, measured by an isotopic tracer technique, was 2.12 +/- 0.17 mM Na+/1 of red blood cells (RBCs)/hr in patients with untreated essential hypertension, compared with 1.55 +/- 0.12 mM Na/1 of RBCs/hr in a group of normotensive controls (p less than .025). Partitioning sodium efflux into ouabain-sensitive and ouabain-insensitive components revealed a significant elevation of both components of membrane sodium transport in the patients with untreated essential hypertension. Ouabain-sensitive sodium efflux was 1.38 +/- 0.09 mM Na/1 RBCs/hr in the patients, compared with 1.04 +/- 0.07 mM Na/1 RBCs/hr in the controls. Ouabain-insensitive sodium efflux was also increased from 0.51 +/- 0.05 mM Na/1 RBCs/hr in the controls to 0.74 +/- 0.09 mM Na/1 RBCs/hr in those with untreated hypertension. Despite these changes in sodium efflux, Na,K-ATPase activity in the erythrocyte membrane, measured at maximum velocity (Vmax), was normal, suggesting that the observed abnormalities in membrane sodium transport in patients with untreated essential hypertension resulted from a change in pump control mechanisms rather than a change in enzyme activity. With the techniques used in this study we were unable to identify changes in erythrocyte membrane transport in the normotensive offspring of hypertensive parents. Membrane sodium transport was also examined in hypertensive patients whose blood pressure had been controlled by medication. In this group it was found that erythrocyte sodium transport did not differ from that in our control group, which suggests that treatment of hypertension can modify fundamental pathophysiologic changes at the level of the cell membrane.
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PMID:Erythrocyte membrane sodium transport in patients with treated and untreated essential hypertension. 630 25

The purpose of this study was to examine proximal and distal tubular function in rats with nonoliguric, myohemoglobinuric acute renal failure (ARF). ARF was induced with glycerol (50%, 10 ml/kg of body wt, i.m.), and renal function was studied 24 hours after glycerol or saline (controls) injection. Glycerol injection caused a 50 to 90% depression in GFR and a significant rise in blood urea nitrogen concentration. Animals with ARF exhibited glycosuria with normal blood sugar levels and a striking depression in tubular glucose reabsorption per milliliter of GFR. The capacity to reabsorb (mEq/liter GFR) was intact at normal blood bicarbonate levels, but was markedly depressed when blood bicarbonate was raised. The tubular maximum for para-aminohippurate (PAH) secretion and the renal extraction fraction of PAH were strikingly depressed in rats with ARF. Distal acidification as assessed by the urine-to-blood gradient of PCO2 (UB PCO2) was normal both during maximal alkalinization of the urine with bicarbonate (urine pH, approximately 7.8) or during neural phosphate infusion (urine pH, approximately 7.0). Net acid excretion per milliliter GFR and minimal urine pH (less than 5.5) following 3 days of ammonium chloride ingestion was similar in control and ARF animals. Potassium excretion was intact in maximal urinary osmolality were significantly altered in animals with ARF. Cortical and outer medullary Na-K-ATPase specific activities were significantly depressed in ARF rats. This occurred as a consequence of enzyme loss and not secondary to alterations in enzyme kinetics of absolute tubular sodium reabsorption. Light and electron microscopy showed diffuse proximal tubular damage, whereas glomeruli and distal tubules were intact. These data demonstrate that glycerol injection produces a diffuse proximal tubular transport defect associated with histologic and enzymatic alterations.
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PMID:Renal tubular function in glycerol-induced acute renal failure. 678 13


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