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)

An N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) displaying the kinetic and pharmacological properties of an electrogenic proton pump has been described in the different segments of rat nephron, where it mediates part of the active tubular proton secretion. This study was therefore designed to evaluate whether changes in urinary acidification observed during metabolic acidosis or alkalosis were associated with alterations of the activity of tubular NEM-sensitive ATPase, and if so, to localize the nephron segments responsible for these changes. Within 1 wk after the onset of ammonium chloride treatment, rats developed a metabolic acidosis, and NEM-sensitive ATPase activity was markedly increased in the medullary thick ascending limb of Henle's loop and outer medullary collecting tubule, and slightly increased in the cortical collecting tubule. Conversely, treatment with sodium bicarbonate induced a metabolic alkalosis that was accompanied by decreased NEM-sensitive ATPase activity in medullary thick ascending limb and outer medullary collecting tubule. NEM-sensitive ATPase activity was not altered in any other nephron segment tested in alkalotic and acidotic rats, i.e., the proximal tubule and the cortical thick ascending limb of Henle's loop. Changes qualitatively similar were observed as soon as 3 h after the onset of NaHCO3 or NH4Cl-loading. In the medullary collecting tubule, alterations of NEM-sensitive ATPase activity are in part due to hyperaldosteronism observed in both acidotic and alkalotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of metabolic acidosis and alkalosis on NEM-sensitive ATPase in rat nephron segments. 131 7

Previous studies have suggested the presence of an H(+)-K(+)-ATPase in rat cortical and medullary intercalated cells with similar properties to the gastric proton pump. The purpose of this study was to determine the functional contribution of an H(+)-K(+)-adenosinetriphosphatase(ATPase) to total CO2 (tCO2) transport along the rat collecting duct. After baseline determination of tCO2 transport in isolated perfused collecting duct segments, Sch 28080 (10 microM) was added to either the perfusate or bath. When Sch 28080 was added to the perfusate, there was no effect in the cortical collecting duct (CCD, 20.8 +/- 6.7 vs. 25.3 + 3.0 pmol.mm-1.min-1), but a marked decrease in tCO2 absorption was effected in both the outer medullary (OMCD, 37.6 + 6.2 vs. 10.7 +/- 4.1 pmol.mm-1.min-1) and initial inner medullary collecting duct (IMCD1, 34.4 +/- 8.1 vs. 16.2 +/- 5.6 pmol.mm-1.min-1). In the CCD from rats with acute alkalosis in vivo, Sch 28080 added to the bath inhibited tCO2 secretion in the CCD (-17.1 +/- 4.4 vs 3.5 + 3.3 pmol.mm-1.min-1). These findings suggest that 1) H(+)-K(+)-ATPase is important in tCO2 absorption in the OMCD and IMCD1 and in tCO2 secretion in the CCD, 2) HCO3(-)-absorbing intercalated cells differ functionally in the cortex and medulla, 3) HCO3- secretion is not the reverse process of HCO3- absorption in the CCD, and 4) H(+)-K(+)-ATPase is important in distal acidification under normal and altered acid-base conditions.
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PMID:H(+)-K(+)-ATPase activity in rat collecting duct segments. 131 8

The present study was designed to test whether tubular carbon dioxide production from the carbon skeleton of uniformly 14C-labelled glutamine exhibits quantitative and qualitative segmental heterogeneity. Our results show that CO2 production from glutamine in the proximal convoluted tubule (PCT) was dependent on substrate concentrations and is saturable at 10(-4) M of glutamine. Glutamine oxidation was demonstrable in all nephron segments examined. The PCT is the quantitatively predominant site of glutamine oxidation. Intermediate nephron segments, however, such as the thick ascending limb (MAL) and the distal convoluted tubule possess a significant capacity for glutamine oxidation, particularly when examined in terms of tubular protein content. Modulation of glutamine oxidation by extracellular pH was segment specific. Stimulation by acidosis and inhibition by alkalosis were observed in the PCT while carbon dioxide production from glutamine in the MAL was pH-insensitive. Glutamine oxidation was closely linked to sodium transport and greatly decreased by inhibition of Na-K-ATPase. In both the PCT and MAL, glutamine oxidation was inhibited by high extracellular potassium concentrations and in the PCT enhanced by extracellular hypokalemia. N-Ethyl maleiamide, an inhibitor of proton ATPase, led to almost complete cessation of CO2 production from the substrate in both PCT and MAL. Acetazolamide, an inhibitor of carbonic anhydrase, led to a partial reduction in carbon dioxide formation in the PCT, but did not affect glutamine oxidation in the MAL. We conclude that segmental qualitative heterogeneity characterizes oxidation of the carbon skeleton of glutamine with proximal segments showing the predictable effects of pH changes and carbonic anhydrase inhibition. The MAL appears to be nonmodulating.
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PMID:Tubular CO2 production from glutamine in the rat: segmental profile and modulation. 137 65

Previous animal and human studies showed that photic stimulation (PS) increased cerebral blood flow and glucose uptake much more than oxygen consumption, suggesting selective activation of anaerobic glycolysis. In the present studies, image-guided 1H and 31P magnetic resonance spectroscopy (MRS) was used to monitor the changes in lactate and high-energy phosphate concentrations produced by PS of visual cortex in six normal volunteers. PS initially produced a significant rise (to 250% of control, p less than 0.01) in visual cortex lactate during the first 6.4 min of PS, followed by a significant decline (p = 0.01) as PS continued. The PCr/Pi ratios decreased significantly from control values during the first 12.8 min of PS (p less than 0.05), and the pH was slightly increased. The positive P100 deflection of the visual evoked potential recorded between 100 and 172 ms after the strobe was significantly decreased from control at 12.8 min of PS (p less than 0.05). The finding that PS caused decreased PCr/Pi is consistent with the view that increased brain activity stimulated ATPase, causing a rise in ADP that shifted the creatine kinase reaction in the direction of ATP synthesis. The rise in lactate together with an increase in pH suggest that intracellular alkalosis, caused by the shift of creatine kinase, selectively stimulated glycolysis.
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PMID:Effect of photic stimulation on human visual cortex lactate and phosphates using 1H and 31P magnetic resonance spectroscopy. 161 37

Calcium plays a pivotal role in cell adhesion, ATPase function, and in membrane permeability. The molecular mechanism for these diverse actions include: hormonal factors, activation of intracellular mediators, and physical factors such as ionic mobility and pH. To further examine the effects of one physical factor, pH, we designed studies examining Ca transport in the isolated turtle bladder epithelium. This tissue is a high-resistance epithelium which reabsorbs Na and secretes H+. The turtle has only rudimentary parathyroid tissue, the gland does not respond to a lowered plasma Ca, and cyclic AMP is not a primary intracellular mediator. In a series of in vitro experiments, we examined Ca metabolism under conditions simulating metabolic acidosis and alkalosis. Acidosis markedly inhibited the mucosa-to-serosa Ca flux, while alkalosis stimulated it. The effect of acidosis on the mucosa-to-serosa Ca flux was independent of Na transport. Changing serosal pH had no effect on the serosa-to-mucosa Ca flux or on proton secretion. Total tissue Ca concentration, measured using atomic absorption spectrometry, was identical when the extracellular pH varied from 5.4 to 8.4. When epithelial cells were isolated and Ca uptake was measured over a wide pH range, a linear increase in uptake was seen as pH was increased from 4.4 to 8.4. In separated turtle bladder epithelial cells ATP-dependent Ca transport, in the mitochondrial-rich cells, was 4- to 5-fold higher than activity found in the granular cells. The mitochondrial-rich cells comprise approximately 20% of the total epithelial surface and are thought to be the cells primarily involved in proton secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium transport and extracellular pH in epithelial membranes. 183 77

The present study was designed to quantitate the amount and to map the localization of N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) activity in microdissected segments of the rat nephron. After complete nephron mapping the effect of chronic metabolic acidosis and alkalosis on enzyme activity was determined. In control animals the highest enzyme activity was found in the early proximal convoluted tubule of juxtamedullary nephrons; superficial early proximal tubule as well as medullary and cortical thick ascending limbs and collecting ducts also contained substantial activity. Enzyme activity in the papillary collecting duct before entry into the ducts of Bellini was 329 +/- 93 pmol.mm-1.h-1 (n = 8); after entry, however, enzyme activity was approximately one-fourth that value (60 +/- 9 pmol.mm-1.h-1, n = 8, P less than 0.01). No NEM-sensitive ATPase activity was found in the thin limbs of the loop of Henle. Enzyme activity increased in both the medullary and cortical thick ascending limbs as well as in the cortical collecting tubule in response to NH4Cl-induced chronic metabolic acidosis; in the cortical collecting duct, metabolic acidosis increased maximum activity (Vmax) but did not change Michaelis-Menten constant (Km). In the proximal convoluted tubule, enzyme activity decreased with metabolic acidosis. Bicarbonate loading had no effect on enzyme activity except in the most distal portion of the collecting duct where it was stimulated. These results show that NEM-sensitive ATPase activity exists throughout much of the rat nephron. These data suggest that both the cortical collecting tubule and thick ascending limb are regulatory sites of distal urinary acidification during acid loading.
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PMID:NEM-sensitive ATPase activity in rat nephron: effect of metabolic acidosis and alkalosis. 213 83

Some functions of dog cardiac sarcoplasmic reticulum have been studied in acidosis and alkalosis conditions in a range of pH from 6.0 to 7.8. Intravesicular water content at pH 6.0 is 4.7 microliter per mg of protein and diminished to 4 microliter, (15%) at pH 8.0; this correlates with a drop of 13.5% in turbidity. Ca2+-dependent ATPase has an optimal pH of 7.2 and a specific activity of 580 nanomoles of ATP hydrolyzed/min/mg protein. The activity of Basal ATPase or Mg2+-dependent is insensitive to changes of pH. Maximal calcium uptake attains 45.1 +/- 1.4 nanomoles per mg protein between pH 6.0 and 6.6. The accumulated calcium diminished progressively when pH was raised. The rate of calcium transport in steady state shows an optimal pH of 6.7. The calcium transport kinetics constants shows that reticulum has a maximal affinity for calcium between pH 6.87 and 7.02. The maximal velocity for transport diminished progressively between pH 6.1 to 7.16. During the calcium transport process pH is changed from acid to alkaline and the accumulated calcium is release proportionally to the pH increment. This effect shows to be reversible. Calcium accumulation and ATP hydrolysis are uncoupled at pH values higher than 6.6 because to the increase in the rate of calcium release. Values of pK and number of protons per mg of protein that dissociates from ionizable residues are 6.53 and 0.68 respectively for calcium dependent ATPase; 7.09 and 0.60 for calcium transport and 7.41 and 0.39 for calcium release. We conclude that the rate of transport and affinity of cardiac sarcoplasmic reticulum for calcium are optimal between pH 6.8 and 7.0 that is the reported range of intracellular pH of normal cardiac tissue. The data are in close agreement with the fall of contractility in acidosis. It is proposed a calcium release pathway sensitive to pH and different from that of calcium pump, exclusively for entrance.
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PMID:[Effects of acidosis and alkalosis on the sarcoplasmic reticulum of the heart]. 293 71

The relationships between pHi (intracellular pH) and phosphate compounds were evaluated by nuclear magnetic resonance (NMR) in normo-, hypo-, and hypercapnia, obtained by changing fractional inspired concentration of CO2 in dogs anesthetized with 0.75% isoflurane and 66% N2O. Phosphocreatine (PCr) fell by 2.02 mM and Pi (inorganic phosphate) rose by 1.92 mM due to pHi shift from 7.10 to 6.83 during hypercapnia. The stoichiometric coefficient was 1.05 (r2 = 0.78) on log PCr/Cr against pHi, showing minimum change of ADP/ATP and equilibrium of creatine kinase in the pH range of 6.7 to 7.25. [ADP] varied from 21.6 +/- 4.1 microM in control (pHi = 7.10) to 26.8 +/- 6.3 microM in hypercapnia (pHi = 6.83) and 24.0 +/- 6.8 microM in hypocapnia (pHi = 7.17). ATP/ADP X Pi decreased from 66.4 +/- 17.1 mM-1 during normocapnia to 25.8 +/- 6.3 mM-1 in hypercapnia. The ADP values are near the in vitro Km; thus ADP is the main controller. The velocity of oxidative metabolism (V) in relation to its maximum (Vmax) as calculated by a steady-state Michaelis-Menten formulation is approximately 50% in normocapnia. In acidosis (pH 6.7) and alkalosis (pH 7.25), V/Vmax is 10% higher than the normocapnic brain. This increase of V/Vmax is required to maintain cellular homeostasis of energy metabolism in the face of either inhibition at extremes of pH or higher ATPase activity.
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PMID:Relationship between intracellular pH and energy metabolism in dog brain as measured by 31P-NMR. 359 78

The structural responses of cells in the distal convoluted, connecting, and collecting tubule to acute acid/base changes were investigated by electron microscopy. Acute metabolic acidosis was induced by administration of ammonium chloride, and acute metabolic alkalosis by potassium or sodium bicarbonate. Morphometric analyses were performed on micrographs of randomly selected distal nephron cells. No structural responses were found in distal convoluted tubule cells, connecting tubule cells, or principal cells but prominent changes were observed in intercalated cells (I cells). Thus, the surface density of the luminal membrane in I cells was significantly higher in acidotic animals and lower in KHCO3 alkalotic animals than in controls. On the contrary, the surface density of the membrane that bounds apical vesicles was higher in KHCO3 alkalotic and lower in acidotic animals than in controls. These results suggest that the luminal membrane is internalized during alkalosis and that the membrane that bounds apical vesicles is transferred to the luminal membrane during acidosis. Since a proton translocating ATPase may be present in the luminal membrane the observations are consistent with the possibility that cortical I cells participate in the maintenance of acid/base homeostasis.
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PMID:Structural adaptation of intercalated cells in rat renal cortex to acute metabolic acidosis and alkalosis. 383 84

Transport systems involved in proximal tubule HCO-3 reabsorption were examined in disaggregated renal cortical tubules from rabbits with metabolic alkalosis. The acid-base disorder was induced by first treating the animals with furosemide, and then maintaining them on low Cl--high HCO-3 diets. On this regimen, the rabbits had increases in blood pH and total CO2 values and decreases in serum K+ concentrations. Urine Cl- concentrations were less than 15 mEq/L in all cases. Na+-H+ exchange was evaluated by incubating tubules in rotenone in an Na+-free medium to deplete them of Na+ and adenosine triphosphate. Then the tubules were resuspended in media containing 65 or 12.5 mEq/L Na+ at either pH 7.1 or pH 7.6. The rise in cell pH estimated by dimethadione distribution was taken as a measure of Na+-H+ exchanger activity. At the high incubation pH, Na+-H+ exchanger activity appeared to be the same in tubules taken from alkalotic rabbits compared with those prepared from normal rabbits. At the low incubation pH, the activity of this transport system appeared to be depressed by 40% to 50% in alkalosis, with kinetics that suggested a decreased Vmax for the exchanger. Na+-independent H+ transport, presumably reflecting activity of an H+-adenosine triphosphatase, was evaluated by preincubating tubules in a Na+-free medium in the presence of ouabain, and then sequentially exposing them to and removing them from a solution containing 20 mmol/L NH4Cl.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proximal tubule hydrogen ion transport processes in diuretic-induced metabolic alkalosis. 400 20


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