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)

Na+ efflux and Na+ tolerance depend on a putative P-type ATPase encoded by the gene ENA1(PMR2) in Saccharomyces cerevisiae and on a putative Na+/H+ antiporter encoded by the gene sod2 in Schizosaccharomyces pombe. This report shows that a sod2::ura4 mutant of S. pombe transformed with the ENA1 gene of S. cerevisiae expressed the ENA1 protein, and recovered Na+ efflux and Na+ tolerance. The efflux of Na+ in the wild strain of S. pombe was sensitive to the transmembrane Na+ and H+ gradients, whereas in the sod2::ura4 mutant transformed with ENA1 it was independent of these gradients. The data give further support to the notion that ENA1 and sod2 encode Na+ transporters and not regulators of the process of Na+ export; they show also the physiological consequences of exporting Na+ through an Na(+)-ATPase or an Na+/H+ antiporter.
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PMID:Functional expression of the ENA1(PMR2)-ATPase of Saccharomyces cerevisiae in Schizosaccharomyces pombe. 772

To examine how uremia changes sodium, potassium, and proton transport, thymocytes from chronic renal failure (CRF) rats were studied. If alterations in cation transport associated with chronic uremia (CRF) extend to intracellular pH regulation, the susceptibility to the catabolic effects of acidosis might be increased. To evaluate the influence of acidosis, cation transport in thymocytes from normal rats with NH4Cl-induced acidosis was also studied. Ouabain-sensitive 86Rb influx in thymocytes from acidotic CRF rats was 32% lower than in control cells (P < 0.05), but intracellular sodium concentration was unchanged. This may be related to a 47 +/- 22% reduction in 22Na influx. In thymocytes from nonuremic, acidotic rats, ouabain-sensitive 86Rb influx was decreased 39% (P < 0.025), similar to the change in CRF. In CRF thymocytes, Na(+)-H+ antiporter activity in response to cell acidification (7.13 +/- 0.8 versus 9.42 +/- 0.8 mmol of H+/L per min; CRF versus control), or to osmotic shrinkage (0.43 +/- 0.09 versus 0.82 +/- 0.11 mmol of H+/L per min; CRF versus control), was significantly (P < 0.01) reduced. Buffering capacity at resting and acidic intracellular pH was unchanged by uremia, but Na+/H+ antiporter activity in response to acid loading or osmotic shrinkage was unchanged in thymocytes of nonuremic rats with metabolic acidosis. Thus, CRF reduces both Na/K-ATPase and Na+/H+ antiporter activities in rat thymocytes. The former may be secondary to reduced sodium influx. Impaired Na+/H+ antiporter activity is not caused by metabolic acidosis alone, whereas reduced Na/K-ATPase activity is found in both acidosis and uremia.
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PMID:Impaired cation transport in thymocytes of rats with chronic uremia includes the Na+/H+ antiporter. 778 58

In recent years, an electrogenic 2Na+/1H+ antiporter has been identified in a variety of invertebrate epithelial brush-border membranes of gut, kidney and gill tissues. The antiporter differs significantly in its physiological properties from the electroneutral 1Na+/1H+ antiporter proposed for vertebrate cells. In all invertebrate cells examined, the antiporter displayed a 2:1 transport stoichiometry, responded to an induced transmembrane potential and exhibited a high binding affinity for the divalent cation Ca2+, which acted as a competitive inhibitor of Na+ transport. A monoclonal antibody specific for the crustacean electrogenic antiporter inhibited 2Na+/1H+ exchange, but was without effect on Na(+)-dependent D-glucose transport. Immunoreactivity was localized at hepatopancreatic brush-border and vacuolar membranes, antennal gland coelomosac podocytes and posterior gill epithelial cells-all locations were published reports described unique cation exchange kinetics. Significant fractions of Ca2+ transport into invertebrate cells across brush-border membranes occurred by an electrogenic, amiloride-sensitive exchange process, probably by the 2Na+/1H+ antiporter, and this transport was markedly inhibited by exogenous zinc and cadmium. A recently identified electroneutral, amiloride-sensitive, hepatopancreatic epithelial basolateral Na+/H+ antiporter was uninfluenced by the brush-border monoclonal antibody, exhibited an apparent 1:1 transport stoichiometry and possessed a minimal divalent cation specificity. Calcium transport at this epithelial pole occurred by the combination of a Ca2+/Na+ antiporter, an ATP-dependent Ca(2+)-ATPase and a verapamil-sensitive calcium channel. These crustacean brush-border and basolateral transporters may play significant roles in calcification and heavy metal detoxification.
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PMID:Role of the invertebrate electrogenic 2Na+/1H+ antiporter in monovalent and divalent cation transport. 782 31

Hyponatremia in cats produced brain edema, detectable by both magnetic resonance imaging (MRI) and increased brain water, with a compensatory decrease of brain sodium. Sodium transport was measured in synaptosomes from hyponatremic cat cerebral cortex. The sodium efflux via Na(+)-K(+)-ATPase was significantly higher (144%) than control, while sodium influx via the Na+/H+ antiporter was significantly decreased (74%). Both responses tend to decrease brain intracellular sodium and thus, brain cell osmolality. Ischemia following unilateral middle cerebral artery occlusion also resulted in brain edema. However, the efflux of sodium via both Na(+)-K(+)-ATPase and sodium channels actually decreased, both maladaptive responses. Furthermore, when ischemia was superimposed upon hyponatremia, all of the cerebral adaptive changes which had been induced by hyponatremia alone were rendered ineffective. This resulted in further elevations of brain water and sodium. Hyponatremia superimposed upon ischemia thus worsens the brain edema associated with ischemia alone. Thus, ischemia impairs the ability of the brain to adapt to hyponatremia, probably by eliminating the compensatory mechanisms of brain sodium transport initiated by hyponatremia.
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PMID:Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia. 797 57

Previous studies have implicated glucocorticoids as an important factor in the postnatal maturational increase in proximal tubule volume absorption, Na+/H+ antiporter, Na(HCO3)3 symporter, and Na(+)-K(+)-ATPase activity. The present study examined whether glucocorticoids are also a potentially important factor in the maturational decrease in proximal tubule phosphate transport. Renal BBMs were prepared from neonatal rabbits who received dexamethasone (10 micrograms/100 g body weight) or vehicle. Brush-border membrane vesicles from dexamethasone-treated neonates had a lower rate of Na-phosphate cotransport than controls (50.8 +/- 3.6 versus 29.2 +/- 2.6 pmol 32P(i)/10 s/mg protein, p < 0.001). This decrease was due to a decrease in the Vmax with no change in the affinity of the transporter for phosphate. The dexamethasone-induced decrease in BBM Na-phosphate transport was not due to a reduction in transporters as assayed by phosphate-protectable Na-dependent equilibrium binding of phosphonoformic acid. Dexamethasone treatment caused an increase in the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene and trimethylammonium-1,6-diphenyl-1,3,5-hexatriene (i.e. a decrease in membrane fluidity). Brush-border membranes from dexamethasone-treated neonates had a decrease in sphingomyelin and an increase in phosphatidylcholine and phosphatidylinositol content but no change in cholesterol or total phospholipid content. These data are consistent with glucocorticoids playing a role in the postnatal maturational decrease in proximal tubule phosphate transport by altering membrane characteristics.
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PMID:Maturational effects of glucocorticoids on neonatal brush-border membrane phosphate transport. 804 84

Neonatal juxtamedullary proximal convoluted tubules (PCTs) transport bicarbonate at one-third the rate of adult rabbit PCTs. The lower rate of bicarbonate transport could be due to a greater permeability of the neonatal PCT to bicarbonate or to a lower rate of active bicarbonate transport. This review discusses potential factors which could result in a lower rate of bicarbonate transport by the neonatal PCT. In isolated perfused PCT, bicarbonate permeability is lower in neonatal than adult PCT, and thus it does not account for the lower rate of bicarbonate transport in neonatal PCT. In the adult PCT, apical proton secretion occurs via the Na+/H+ antiporter and H(+)-ATPase; basolateral bicarbonate exit occurs via the Na(HCO3)3 symporter. The activity of transporters can be ascertained by measuring intracellular pH with the fluorescent dye BCECF. Apical Na+/H+ antiporter, apical H(+)-ATPase and basolateral Na(HCO3)3 symporter activity are all significantly lower in neonatal PCT. The factors which stimulate PCT maturation are unknown, however glucocorticoids have been postulated to play an important role in this process. Administration of dexamethasone to pregnant does results in higher rates of PCT volume absorption, bicarbonate transport, Na+/H+ antiporter and Na(HCO3)3 symporter activities than in PCT from vehicle-treated controls. Thus, the lower rate of neonatal PCT bicarbonate transport is due to lower activities of the apical Na+/H+ antiporter, apical H(+)-ATPase and basolateral Na(HCO3)3 symporter. Glucocorticoids may be an important factor in the maturation of PCT acidification.
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PMID:Maturation of proximal tubular acidification. 813 Jan 10

Leishmania donovani has an active K+/H+ exchange system on the surface membrane. Modulation of external K+ concentration resulted in a corresponding change in internal pH (pHi) suggesting a link between proton and potassium transport. Although a Na+/H+ antiporter is present on the plasma membrane, its sensitivity to amiloride suggests that it operates independent of K+/H+ exchange. Reduction of cellular ATP with NaN3 and KCN inhibits K+/H+ exchange showing thereby that the process is energy dependent. The K+/H+ exchange is sensitive to inhibitors of the gastric K+/H(+)-ATPase. It is concluded that the H(+)-ATPase previously reported on the plasma membrane of L. donovani is in fact a K+/H(+)-ATPase.
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PMID:Plasma membrane K+/H(+)-ATPase from Leishmania donovani. 813 91

Abnormal growth of vascular smooth muscle (VSM) is seen in various pathologic conditions such as hypertension and atherosclerosis. Many classic vasoconstrictors have now been shown to be mitogenic, either by themselves or in conjunction with other cofactors, such as insulin. The mitogenic effects of vasoconstrictors may be due, in part, to activation of similar second messenger pathways, including stimulation of the Na+/H+ antiporter. It has been suggested, therefore, that an enhanced proliferation rate may be, in part, the consequence of elevated Na+/H+ exchange. This hypothesis is supported by several observations of the close association between Na+/H+ exchange activity and DNA synthesis in some cell types including fibroblasts and VSM. Stimulation of Na+/H+ exchange may play a permissive role in optimal growth by preventing H+ accumulation (a fall in intracellular pH [pHi]) due to the increased metabolic activity during cell stimulation. Enhancement of Na+/H+ exchange activity increases Na+ influx into the cell, and secondarily increases K+ entry through activation of Na+/K+ ATPase activity. Although the Na+/H+ antiporter may influence cell proliferation through various ionic mechanisms, it is not clear that enhanced proliferation is the consequence of overactivity of this antiporter. In VSM, there are also differences in the pattern of activation of the Na+/H+ antiporter by hyperplastic and hypertrophic agents. Although pHi is increased in response to both acute and chronic stimulation by hyperplastic factors, such as platelet-derived growth factor, a hypertrophic agonist such as angiotensin II increases pHi acutely but lowers it chronically. Likewise, hyperplastic factors increase the Na+/H+ antiporter (NHE-1) mRNA levels, whereas angiotensin II does not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na+/H+ exchange and vascular smooth muscle proliferation. 814 Nov 73

The ATP-supported 22NA+ uptake by plasma membrane vesicles from the marine microalga, Platymonas viridis, was studied. At pH 7 in the medium, Na+ uptake did not occur in the presence of ATP although delta pH across the plasma membrane was generated. The ATP-dependent Na+ uptake was induced by adding the protonophore, ClCCP. At pH 8, Na+ uptake took place when ATP was added even without ClCCP. The delta pH generated across the plasma membrane was negligible under these conditions. The Na+ uptake at pH 8 was not affected by ClCCP and amiloride, an inhibitor of the Na+/H+ antiporter. It is concluded that the ATP-supported Na+ uptake by Pl. viridis vesicles is catalyzed by Na(+)-ATPase.
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PMID:The ATP-driven Na(+)-pump in the plasma membrane of the marine unicellular alga, Platymonas viridis. 816 19

The purpose of this study was to characterize the role of ions other than Ca2+ in hepatic responses to alpha 1-adrenergic stimulation. We report that the alpha 1-adrenoreceptor activation of hepatic functions is accompanied by extracellular acidification and an increase in intracellular pH. These effects are dependent on extracellular Na+ concentration and are inhibited by the Na+/H+ antiporter blocker 5-(N-ethyl-N-isopropyl) amiloride under conditions that preclude antagonistic effects on agonist binding. Thus, the activation of plasma membrane Na+/H+ exchange is an essential feature of the hepatic alpha-adrenoreceptor-coupled signaling pathway. The following observations indicate that the sustained hepatic alpha 1-adrenergic actions rely on a functional coupling between the plasma membrane Na+/H+ and Na+/Ca2+ exchangers, resulting in the stimulation of Ca2+ influx. 1) Inhibition of the Na+/K(+)-ATPase does not prevent the alpha 1-adrenergic effects. However, alpha 1-adrenoreceptor stimulation fails to induce intracellular alkalinization and to acidify the extracellular medium in the absence of extracellular Ca2+. 2) A non-receptor-induced increase in intracellular Na+ concentration, caused by the ionophore monensin, stimulates Ca2+ influx and increases vascular resistance. 3) Inhibition of Na+/Ca2+ exchange prevents, in a concentration-dependent manner, most of the alpha 1-agonist-induced responses. 4) The actions of Ca(2+)-mobilizing vasoactive peptide receptors or alpha 2-adrenoreceptors, which produce neither sustained extracellular acidification nor release of Ca2+, are insensitive to Na+/H+ exchange blockers.
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PMID:Functional coupling of Na+/H+ and Na+/Ca2+ exchangers in the alpha 1-adrenoreceptor-mediated activation of hepatic metabolism. 828 39


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