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)

It is proposed that the energy-transducing system of the first cellular organism and its precursor was fueled by the oxidation of hydrogen sulfide and ferric sulfide to iron pyrites and two [H+] on the outside surface of a vesicle (the cell membrane), with the concomitant reduction of CO or CO2 on the interior. The resulting proton gradient across the cell membrane provides a proton-motive force, so that a variety of kinds of work can be done. It is envisioned as providing a selective advantage for cells capable of harvesting this potential. The proposed reactants for these reactions are consistent with the predicted composition of the Earth's early environment. Modern-day homologs of the ancestral components of the energy-transducing system are thought to be membrane-associated ferredoxins for the extracellular redox reaction, carbon monoxide dehydrogenase for the carbon fixation reaction, and ATPase for the harvesting of the proton gradient. With a source of consumable energy, the cell could drive chemical reactions and transport events in such a way as to be exploited by Darwinian evolution.
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PMID:The first cellular bioenergetic process: primitive generation of a proton-motive force. 166 58

The Ca2+ dependence of muscarinic-induced fluid and electrolyte secretion was studied using rat sublingual mucous gland preparations. During stimulation, secretions from vascularly perfused glands were totally inhibited when perfused with a Ca(2+)-free medium. Fluid secretion correlated with sustained losses of 42K+ and 36Cl- content and sustained increases in 22Na+ content and the intracellular free Ca2+ concentration ([Ca2+]i) in fura-2-loaded acini. The magnitudes of the initial agonist-induced changes in Na+, K+, and Cl- content and [Ca2+]i were unaltered in a Ca(2+)-free medium, whereas extracellular Ca2+ removal resulted in the recovery of these ions during the sustained phase to pre-stimulation levels. The recovery of Cl- content induced by Ca2+ depletion was totally blocked in the presence of bumetanide, an inhibitor of Na(+)-K(+)-2Cl- cotransport, while 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of anion exchange, did not influence Cl- recovery in a HCO(3-)-containing solution (25 mM NaHCO3, 5% CO2). The stimulated increase in [Ca2+]i was not inhibited by the addition of voltage-activated Ca2+ channel blockers (D 888, nifedipine, and diltiazem) or in a Na(+)-free medium. Studies using the quench of fura-2 by Mn2+ as an index of Ca2+ influx and thapsigargin, an inhibitor of microsomal Ca(2+)-ATPase, indicate that a capacitative Ca2+ entry pathway mediates Ca2+ entry during stimulation. The above data demonstrate that Ca2+ uptake, which is dependent on the refill status of the agonist-sensitive intracellular Ca2+ pool, is a prerequisite for sustained muscarinic-induced fluid and electrolyte secretion in the rat sublingual mucous gland.
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PMID:A capacitative Ca2+ influx is required for sustained fluid secretion in sublingual mucous acini. 172 46

An increase in ambient CO2 tension from 3% to 11% augments colonic Na absorption in the rat. The membrane site of action of CO2 was examined by measuring colonic Na absorption in the Ussing chamber when nystatin was used to permeabilize the luminal (apical) membrane. The equal rates of ouabain-sensitive Na absorption at 3% and 11% CO2 in the presence of nystatin and at 11% CO2 in its absence suggested that CO2 acted at the luminal membrane. This finding was also observed at a submaximal rate of Na absorption (produced by lowering bathing solution Na from 140 to 27 mmol/L) and in a Cl-free solution (to prevent cell swelling). The basolateral membrane was indeed rate limiting for Na absorption in the presence of nystatin, because methylprednisolone (3 mg/kg SC for 3 days to increase sodium-potassium--stimulated adenosine triphosphatase activity) increased Na absorption measured in the presence of nystatin and because CO2 increased absorption in steroid-treated rats in the absence of nystatin. These results validate the protocol and confirm the luminal site of action of CO2 and nystatin on colonic Na absorption.
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PMID:Effect of CO2 on rat colonic Na absorption: studies with nystatin. 172 83

The progress of research in the Central Nervous System (CNS) had led to the consideration of neurons and glia as indissociable functional complexes. Neuron-glia interactions are essential for the maturation of the CNS. Glial cells release trophic factors for neurons (NGF) and neurons release trophic factors for glia (GGF). Furthermore, the latter provide a substrate for the migration of neurons and guidance of axons by mean of adhesion molecules. In adults, the interactions between neurons and glial cells serve to maintain homeostasis. Thus, the glial cells perform the restoration of the metabolic equilibrium overthrown by the transmission of the nerve impulse and provide the glucose required for neuronal activity. The nerve impulse provokes increases in the cellular space of CO2, K+, NH3 and neurotransmitters which must be taken up to allow neuronal activity to continue (in normal conditions). Astrocytes perform the uptake of the extracellular K+ by means of passive ionic channels, ionic voltage-dependent channels and a sodium-potassium-ATPase-dependent pump. The oligodendrocytes are involved in the metabolism of CO2 by converting CO2 into carbonic acid by means of carbonic anhydrase. Oligodendrocytes and astrocytes play a role in terminating neural transmission by the uptake of the amino acid neurotransmitters, such as GABA, glutamate and aspartate. The catabolism of glutamate to glutamine by means of glutamine synthetase allows both the conversion of an excitatory amino acid into a neutral amino acid (which can diffuse in the extracellular space without causing neural transmission) and the reduction of cerebral NH3 content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuron-glia interactions]. 178 93

Mineralocorticoid steroids markedly alter ion transport in responsive epithelia. Increases in absorption of Na+ and secretion of K+ and H+ are accompanied by increases in surface area of the basolateral membrane. The basolateral membrane changes are associated with increased Na(+)-K(+)-ATPase activity and increased numbers of Na(+)-K(+)-ATPase pump sites. It is thought that H+ secretion is mediated by H+ pumps contained in apical vesicles that are added to the luminal membrane in response to acidifying stimuli. Whether there are changes in the number or volume of apical vesicles in response to aldosterone has not been evaluated. To this purpose, we evaluated apical membrane morphology in rat distal colon, a mineralocorticoid-responsive epithelium. We found that aldosterone infused for 4-7 days by osmotic minipump significantly increased the number, surface density, and total volume of apical vesicles. Exposure of tissues to 5% CO2 for 15 min before fixation resulted in significant decreases in vesicle number, surface density, and volume in aldosterone-stimulated tissues. After CO2, apical vesicles in aldosterone-stimulated tissues tended to be closer to the luminal membrane; apical membrane surface density was increased but not to a significant degree. Fluorescence microscopy demonstrated acridine orange accumulation in discrete points under the lumen, suggesting the presence of acidic vesicles in this location. We propose that aldosterone increases the activity of a membrane shuttle system that is regulated by CO2 as found in other H(+)-secreting epithelia. This system may mediate aldosterone-induced changes in colonic H+ transport.
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PMID:Aldosterone induces apical vesicles in rat distal colon. 211 40

Changes in systemic acid-base balance are known to influence acidification in the collecting duct. The H+ secretion in the collecting duct has been shown to be an electrogenic process and it has been suggested that an H-ATPase sensitive to inhibition by N-ethylmaleimide (NEM) is responsible for H+ secretion. This study was designed to determine the effect of metabolic alkalosis on NEM-sensitive ATPase activity in the microdissected segments of the distal nephron. Metabolic alkalosis was produced by giving NaHCO3 to normal rats for 7 days. The plasma total CO2 concentration in the experimental group was 31.5 +/- 1.8 mM compared with 23.4 +/- 1.0 mM in the control group. NEM-sensitive ATPase activity was significantly lower in the cortical collecting duct and in the outer and inner medullary collecting ducts of alkali-loaded rats than those of control rats. There was no significant difference in the enzyme activity between the two groups of animals in the other nephron segments examined. Our results suggest that NEM-sensitive H-APTase activity in all three segments of the collecting duct is modulated by the acid-base status of the animal.
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PMID:Decrease in N-ethylmaleimide-sensitive ATPase activity in collecting duct by metabolic alkalosis. 214 64

The production of 14CO2 from uniformly labeled glucose was shown to account for the entire increase in histamine-stimulated O2 consumption in rabbit gastric glands when no other substrate was added to the medium. The increased production of CO2 was correlated to the increase in O2 consumption and the accumulation of [14C]-aminopyrine (AP) after stimulation with several secretagogues. Inhibitors of H(+)-K(+)-ATPase reduced the secretagogue-induced increase in CO2 production by greater than 90%, showing that the activity of this enzyme was responsible for the greater part of gastric gland metabolism under stimulated conditions. In contrast to AP accumulation, inhibition of CO2 production by omeprazole, an acid-activated inhibitor of the H(+)-K(+)-ATPase, was not reversed by washing. The reversal of AP accumulation after omeprazole treatment and washing was most likely due to a recruitment of residual pumps bordering a nonacidic space, which had not previously been inhibited by omeprazole. These residual pumps slowly generate a pH gradient and hence AP uptake. Adding NH4+ to gastric glands resulted in a concentration-dependent increase of CO2 production up to the maximal stimulated level but without formation of the pH gradient as measured by AP uptake and loss of the omeprazole inhibition of glucose oxidation. As NH4+ can act as a K+ surrogate for H(+)-K(+)-ATPase, and as NH3 is membrane permeant, full stimulation of CO2 production is evidence that the major mechanism of H(+)-K(+)-ATPase activation in situ is an increase in the KCl permeability of the pump membrane.
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PMID:Coupling of H(+)-K(+)-ATPase activity and glucose oxidation in gastric glands. 215 39

Although numerous studies have documented the effects of the renal nerves on kidney function, the mechanisms involved in the diuresis have yet to be elucidated. The present study was undertaken to examine the effect of acute unilateral renal denervation (DNX) on proximal tubular absorption of fluid and bicarbonate and to determine if acute DNX was associated with changes in Na-K-ATPase activity. Acute DNX caused significant increases in urine flow and absolute and fractional excretions of Na, HCO3 and K compared to the contralateral control kidney (INN) or sham denervated kidneys in normal rats as well as in rats made alkalotic by the I.V. infusion of 150 mM NaHCO3. These effects were seen without significant changes in GFR. When proximal convoluted tubules (PCT) were perfused with bicarbonate-Ringer's solution DNX resulted in a 67% decrease in fluid reabsorption (INN: 3.0 +/- 0.2 vs DNX: 1.0 +/- 0.1 nl/min/mm; p less than 0.001) and a 40% decline in bicarbonate (total CO2) reabsorption (INN: 151.3 +/- 8.8 vs DNX: 94.5 +/- 10.1 pmol/min/mm; p less than 0.01). Acute DNX caused a significant reduction in Na-K-ATPase activity measured in microsomes derived from the outer cortex of the kidney (INN: 13.2 +/- 1.3 vs DNX: 10.9 +/- 0.7 mumol PO4/mg prot/hr; p less than 0.01) while Mg-ATPase was unaffected. Sham denervation had no effect on any of the above parameters. These results indicate that the renal nerves play an important role in the regulation of bicarbonate and fluid reabsorption in the PCT. The diuresis, natriuresis, and bicarbonaturia associated with acute unilateral renal denervation may be the direct result of inhibition of Na-K-ATPase activity.
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PMID:Sodium and bicarbonate reabsorption in microperfused proximal tubules from the denervated rat kidney: relationship to cortical Na-K-ATPase activity. 217 83

Turtle urinary bladder possesses four ion transport processes: Na+ absorption, H+ secretion, and HCO3- secretion-Cl- absorption. Each transport process is performed by a specific epithelial cell type. Granular cells absorb Na+ but they are not sensitive to antidiuretic hormone (ADH), unlike toad bladder granular cells. alpha-Carbonic anhydrase-rich (CA) cells secrete H+ via an apical H+-adenosinetriphosphatase (ATPase). Under conditions of low CO2 tension, this active pump is contained in the limiting membranes of certain cytoplasmic vesicles. The vesicles fuse with the apical membrane, and H+ pumps are incorporated into that membrane, as physiological conditions demand increased H+ secretion. The stimulus for fusion of these vesicles with the apical membrane appears to be intracellular acidification. beta-CA cells secrete HCO3- and reabsorb Cl-, both processes driven by H+-ATPase in the basolateral membrane in series with an apical Cl- -HCO3- exchanger. Increased intracellular adenosine 3',5'-cyclic monophosphate concentration in beta-cells stimulates net HCO3- secretion and induces an electrogenic component of this flux by activating an apical Cl- channel. This activation accompanies the fusion of an intracellular tubulovesicular network with the apical membrane. The membrane of this network may contain Cl- channels.
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PMID:Turtle urinary bladder: regulation of ion transport by dynamic changes in plasma membrane area. 251 70

To study proximal tubule bicarbonate absorption that is not due to the neutral Na+-H+ antiporter, mid to late proximal convolutions of the rat kidney were microperfused in vivo with a sodium-free choline solution containing 10(-3) M amiloride. The average sodium concentration resulting from sodium influx was 12 mM. At such low intraluminal [Na+], 10(-3) M amiloride should have inhibited the Na+-H+ antiporter by greater than 95%. When 25 mM HCO3- was in the perfusion fluid, measured total CO2 absorption was 100 pmol.mm-1.min-1. When luminal [HCO3-] was raised to 50 mM, and blood [HCO3-] was also raised to approximately 50 mM to avoid a transepithelial HCO3- concentration gradient, total CO2 absorption increased to greater than 300 pmol.mm-1.min-1. Thus raising intraluminal HCO3- concentration caused a marked increase in total CO2 absorption even though intraluminal [Na+] was low and amiloride was present. Control perfusions containing 140 mM Na+ yielded total CO2 absorption that was approximately 100 pmol.mm-1.min-1 higher than with the respective sodium-free perfusion solutions. In additional experiments, either DCCD or NEM was added to sodium-free perfusion solutions to inhibit H+-ATPase. These inhibitors reduced Na+-H+ independent total CO2 absorption markedly. Our observations suggest that under physiological acid-base conditions, sodium-independent H+ secretion can account for approximately 50% of total HCO3- absorption in mid to late proximal convolutions. This mechanism is stimulated by an increase in ambient HCO(-3) concentration to a degree that might account for the load-dependency of proximal HCO(-3) absorption in these segments of the proximal tubule.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proximal bicarbonate absorption independent of Na+-H+ exchange: effect of bicarbonate load. 253 46


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