Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synaptosomes, or nerve-ending particles, were isolated from the cerebral cortices of young rats by homogenization, differential centrifugation, and density-gradient centrifugation. The sodium-potassium-activated adenosine triphosphatase enzyme system [(Na+ plus K+)-ATPase] of these particles is believed to represent in vitro the sodium-potassium pump of the nerve terminal. Suspensions of synpatosomes were equilibrated with air containing various concentrations of halothane and enflurane, as determined by gas chromatography. Clinical concentrations of the anesthetics had no effect on (Na+ plus K+)-ATPase activity. Fourteen per cent halothane and 14.8 per cent enflurane in the gas phase resulted in 12 and 10 per cent inhibition, respectively, of (Na+ plus K+)-ATPase activity. These data confirm that interference with active cation transport by inhibition of neuronal (Na+ plus K+)-ATPase is not related to the mechanism of halothane or enflurane anesthesia. (Key words: Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Metabolism, enzymes, ATPase; Nerve, synaptosomal ATPase; Theories of anesthesia, ATPase.).
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PMID:The effects of halothane and enflurane on rat brain synaptosomal sodium-potassium-activated adenosine triphosphatase. 80 97

Proximal convoluted tubules were dissected from rabbit kidneys and perfused in vitro in order to determine the effect of monovalent ions on fluid absorption and transepithelial voltage. Replacement of sodium in the perfusate and bath by lithium, tetramethyl ammonium or choline caused the rate of fluid absorption and voltage to fall to near zero. Replacement of potassium in the bath by sodium had the identical effect. Replacement of chloride by nitrate or perchlorate had comparatively little effect. The results are consistent with the generally held view that active sodium transport (mediated by a Na- and K- activated adenosine triphosphatase) is the primary process responsible for the absorption of the fluid and the voltage. Replacement of bicarbonate in the perfusate and bath by chloride caused the rate of fluid absorption to decrease by 33%. The possible relation between sodium transport and bicarbonate is discussed.
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PMID:Role of monovalent ions in the reabsorption of fluid by isolated perfused proximal renal tubules of the rabbit. 97 42

Ethanol (3%) decreases the potential difference and short-circuit current across the isolated frog skin in chloride Ringer's solution. Unidirectional fluxes of Na and Cl indicate that the drop in short-circuit current is due to an inhibition of the sodium influx. However, ethanol had no effect on the electrical parameters or sodium fluxes, when the frog skin was bathed in chloride-free solutions on both sides or the outside alone. The ethanol response is anion-dependent. In addition, chloride-free media in the inside bathing solution reduced the short-circuit current, indicating a sodium transport pathway which is dependent on chloride and confirming previous data in the literature. Other anions such as sulfate and nitrate could not substitute for chloride. The vasopressin-induced natriferic response and the ethanol effect were found to work independently of each other and different pathways of action are suggested for these agents. The intracellular sodium content of the isolated frog skin epithelium increased and potassium decreased in the presence of the Na-K adenosine triphosphatase inhibitor, ouabain, whereas ethanol or amiloride had no effect. The oxygen consumption of the isolated frog skin was unaffected by up to 10% ethanol. A general metabolic action is probably thus not mediating the response. Urea, in iso-osmotic concentrations to the ethanol, did not mimic its effect. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. It is suggested that ethanol may impede the flow of water across frog skin by a physicochemical interaction with membrane pores and the water molecules. The permeability coefficient (Ktrans) for ethanol was found to be 10 times smaller than the Ktrans for water.
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PMID:Effects of ethanol on the permeability of frog skin. 108 5

A patient with excessive industrial exposure to silicon and an elevated silicon content in his renal tissue was found to have a distinctive nephropathy, characterized pathologically by changes in the glomeruli and proximal tubules, and manifested clinically by albuminuria and hypertension. Proximal tubular function was intact. From a biochemical standpoint, this finding correlates with the demonstration in vitro that, in contrast to cadmium, a known cause of Fanconi syndrome, silicon does not inhibit renal cortical sodium-potassium-adenosine triphosphatase (Na-K-ATPase).
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PMID:Silicon nephropathy. 113 57

The effects of norepinephrine in interaction with adrenergic blocking compounds were studied on membrane adenosine triphosphatase (ATPase) activities of human lymphocytes and lymphoblasts. Sodium-potassium ion exchange pump activity was assayed by 86-Rb uptake and ATPase activity of membrane fractions was assayed by ADP and inorganic phosphate generation. The results of these studies indicate that norepinephrine acts by an alpha adrenergic mechanism to enhance membrane sodium-potassium ion exchange pump activity and ATPase activity. The pharmacologic and ionic dissection of the adrenergic sensitivity of ATPase activity indicates that this alpha adrenergic mechanism is related to membrane ATPase activities in addition to that associated with the ion exchange pump. Analysis of fractions obtained by sucrose gradients indicates that the action of norepinephrine is localized in the plasma membrane. Beta adrenergic stimulation was observed to inhibit ATPase activity. The complexity of adrenergic effects on membrane ATPase suggests interactions of hormone modulation of membrane nucleotide cyclases and transport-related ATPase enzymes.
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PMID:Norepinephrine stimulation of lymphocyte ATPase by an alpha adrenergic receptor mechanism. 114 Jan 64

Dogs were bled and maintained at an arterial pressure of 6.7 kPa for 3 hours. During hemorrhagic shock, red blood cell and serum were assayed for Na+, K+ and Ca++ ion level. RBC and hepatic tissue were together assayed for adenosine triphosphatase (ATPase) activities, free radicals. Results showed that: (1) at 15 minutes after hemorrhagic shock. ATPase activities in RBC and hepatic tissue was significantly elevated. While ratio of sodium and potassium (Na+/K+) in RBC was showed no significant difference; (2) ATPase activities in RBC and liver were decreased, Na+/K+ in RBC was elevated at first after hemorrhagic shock; (3) the signals of free radicals were increased during hemorrhagic shock. The signals of free radicals and ATPase activities in cell membrane was negative correlated. While signals of free radicals and Na+/K+ in RBC was positive correlated. Based on these findings, it is proposed that: free radicals after hemorrhagic shock is an important factor responsible for decrease of ATPase activities and dysfunction of ions active transport in cell membrane.
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PMID:[An experimental study on the mechanism of impairment of cell membrane during hemorrhagic shock in dogs]. 132 74

Principally to ascertain whether mineral metabolism is involved in weight regulation, the 40 most obese of 1,774 children, aged 10-11 years, screened for obesity were compared with 46 age-matched controls. The obese children had more 3H-Ouabain erythrocyte binding sites (p = 0.04), higher intracellular sodium (p = 0.04), and lower plasma sodium (p = 0.002). After exclusion of the non-Scandinavians, the p values were p = 0.02, p = 0.03, and p = 0.03, respectively. Analysis of variance also showed the differences to be more dependent on obesity than on gender or nationality. It is concluded that obese children have more 3H-Ouabain erythrocyte binding sites indicating an increase of the sodium-potassium adenosine triphosphatase activity. The increase of intracellular sodium may increase the risk of future hypertension.
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PMID:Red cell sodium-potassium adenosine triphosphatase sites and intracellular sodium increased in obese school children. 132 34

Cholesterol oxidation products (oxysterols), such as cholestan-3 beta,5 alpha,6 beta-triol (Triol), may be atherogenic by altering the barrier function of the vascular endothelium. We have shown that incubation of endothelial cell monolayers with Triol increased transendothelial albumin transfer (i.e., decreased barrier function) in a concentration- and time-dependent manner. Such dysfunction of endothelium could result from alterations in membrane characteristics, including changes in membrane-associated enzyme activities. To test this hypothesis, endothelial monolayers were treated with 20 microM Triol and the activities of selected membrane enzymes were measured at 0, 2, 4, 6, 12 and 24 hours. Calcium-adenosine triphosphatase (Ca(++)-ATPase) and sodium, potassium, magnesium-adenosine triphosphatase (Na+, K+, Mg(++)-ATPase) activities were significantly increased after 4 or 2 hours incubation with 20 microM Triol, respectively. 5'-nucleotidase activity was significantly elevated only after a 24-hour exposure to Triol, whereas there was no change in angiotensin-converting enzyme (ACE) activity in response to 20 microM Triol treatment at any time studied. Compared with all concentrations tested 40 microM Triol increased Ca(++)-ATPase activity most markedly, with a significant increase already after a 2-hour exposure. No major morphological changes were noted until 12 hours of exposure to 20 microM Triol; obvious cellular damage was observed by 24 hours. Cultures treated with Triol for 24 hours showed significant signs of toxicity, measured by an elevated [3H]adenine release, compared with control cultures. These data demonstrate that Triol alters the activity of certain membrane-bound enzymes, particularly Na+, K+, Mg(++)-ATPase and Ca(++)-ATPase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxysterol-induced endothelial cell dysfunction in culture. 133 99

The perilymphatic compartment of the inner ear resembles plasma ultrafiltrate, whereas the endolymphatic compartment is characterized by a high potassium and low sodium concentration. Perilymph is considered to be the precursor of endolymph. The chemical composition of endolymph and the generation of the transepithelial potential is regulated by Na-K-activated adenosine triphosphatase. The cytochemical localization of Na/K ATP-ase is demonstrated in the guinea pig inner ear. The mechanism for cation regulation in the endolymphatic compartment is discussed.
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PMID:[Localization of Na/K ATP-ase in the inner ear]. 133 29

We studied the cellular membrane enzyme responsible for potassium transport in different Thai populations. We measured plasma and intraerythrocytic concentrations of sodium and potassium, activities of erythrocytic membrane Na, K-activated adenosine triphosphatase (Na, K-ATPase), ouabain-insensitive ATPase, total ATPase and the activity ratio of Na, K-ATPase/total ATPase in 25 healthy blood donors at Khon Kaen University Hospital, Khon Kaen (group 1), and in 32 donors at the National Blood Center, Thai Red Cross Society, Bangkok (group 2). Group 1 subjects had significantly higher concentrations of erythrocyte sodium (p < 0.001) and lower activity of Na, K-ATPase (p < 0.001) than group 2. When data of these 2 groups were combined, erythrocyte Na+ correlated inversely with Na, K-ATPase and the activity ratio of Na, K-ATPase/total ATPase. Our study suggests that there is a defect in membrane transport enzymes for sodium/potassium in certain northeast Thai populations.
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PMID:Abnormal erythrocyte Na, K-ATPase activity in a northeastern Thai population. 133 1


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