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)

The present study was aimed to investigate whether the promoting activity of phenobarbital in rodent liver is related to its daily dose level and duration of treatment or rather to its total dose administered. For this purpose groups of female Wistar rats were treated for 5 consecutive days with an initiating dose of 10 mg/kg body weight N-nitrosodiethylamine. Subsequently, rats were given phenobarbital-sodium (PB) in their drinking water at concentrations of 20, 50, 100 and 200 mg/l for varying lengths of time, such that the total dose of xenobiotic was very similar throughout the different treatment groups ranging from approximately 950 to 1100 mg/kg body weight. The number and volume fraction of lesions negative for the marker enzyme adenosine triphosphatase in liver were subsequently scored as a means to determine the carcinogenic response in this organ. Slight promoting effects of PB were only seen at the lowest concentration of 20 mg/l, whereas no significant effects were observed at 50 and 100 mg/l. At the highest concentration of 200 mg/l an inhibition of carcinogenic response was obtained. Although the effects seen in this study were only moderate, our data favour the idea that the promoting effects of PB depend on the actual concentration of the compound and the duration of treatment rather than on the total dose administered.
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PMID:Effect of varying the concentration of phenobarbital and its duration of treatment on the evolution of carcinogen induced enzyme-altered foci in rat liver. 182 59

Prostacyclin (PGI2) did not alter the basal perfusion pressure in the isolated rat mesenteric arteries perfused with Krebs' solution, but produced a biphasic effect in arteries preconstricted with norepinephrine or arginine vasopressin: constriction, then prolonged dilation. Both these components of PGI2 effect were diminished in arteries denuded of their endothelia by a 10 min perfusion with distilled water or p-bromophenacyl bromide (10 microM). The present study elucidates the mechanism of these PGI2 actions. Indomethacin (0.28 microM) SQ 29548 (1 microM, thromboxane A2 receptor antagonist), saralasin (1 microM, angiotensin II receptor antagonist) or the free radical scavengers, superoxide dismutase (60 U/ml) and catalase (40 U/ml) did not inhibit the initial vasoconstriction, suggesting it was not mediated through endothelially generated thromboxane A2, angiotensin II or oxygen-derived free radicals. However, ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (50 microM; Ca++ chelating agent), 8-(diethyl-amino)octyl 3,4,5-trimethoxy benzoate (10 microM; intracellular Ca++ antagonist), or neomycin (5 mM; phospholipase-C inhibitor) abolished the vasoconstriction. Ouabain (0.5 mM) did not affect the vasodilation, but perfusion with excess (50 mM) or 0 K+ Krebs' solution abolished it, suggesting this PGI2 action involves changes in membrane K+ conductance via a mechanism independent of Na+/K+ adenosine triphosphatase. Vasodilation evoked by BRL 34915 (K+ channel activator) was similarly attenuated under these conditions, but not by ouabain. Furthermore, procaine (1 mM; nonspecific K+ channel inhibitor), but not apamin (0.5 microM) or tetraethylammonium (10 mM) blocked PGI2- and BRL 34915-induced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of vascular actions of prostacyclin in the rat isolated perfused mesenteric arteries. 210 93

1. We have used n.m.r. spectroscopy to measure rubidium concentrations in the skeletal muscle of live intact rats. Using a 1.9 T superconducting magnet and an ear-phone coil tuned to both protons (1H) and rubidium (87Rb), it was possible to make measurements of both tissue rubidium content and water content, and from these measurements to obtain the rubidium concentration. 2. The n.m.r. estimate of rubidium concentration in muscle in vivo was found to be a constant 31% (SEM 4%) of that estimated by flame atomic absorption spectroscopy in an extract of excised muscle. This is close to the predicted theoretical n.m.r. visibility of 33%. The visibility was constant for muscle rubidium concentrations ranging between 10 and 34 mmol/l. 3. Rubidium concentration measurement by this method is unaffected by variations in sample geometry, sample volume, tissue conductivity, coil tuning and amplifier gain. 4. By using this method to measure changes in tissue rubidium concentration with time in the same animal, it should now be possible to assess the activity of ion transport systems, such as sodium- and potassium-activated adenosine triphosphatase in vivo, by measuring the rates of change of tissue rubidium concentrations during the administration of rubidium salts. 5. This method could also be used to measure the absolute concentration of any n.m.r.-visible nucleus and could be applied to man.
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PMID:A non-invasive method of measuring concentrations of rubidium in rat skeletal muscle in vivo by 87Rb nuclear magnetic resonance spectroscopy: implications for the measurement of cation transport activity in vivo. 215 50

The mechanism of action of aloe-emodin-9-anthrone, a decomposition product of barbaloin, in causing a significant increase in the water content of the rat large intestine, was investigated. Aloe-emodin-9-anthrone inhibited rat colonic Na+, K(+)-adenosine triphosphatase (ATPase) in vitro, and increased the paracellular permeability across the rat colonic mucosa in vivo. Therefore, it seemed that the increase in water content of the rat large intestine produced by aloe-emodin-9-anthrone was due to both inhibition of absorption and stimulation of secretion without stimulation of peristalsis. Furthermore, pretreatment with loperamide, an antidiarrheal agent, completely prevented the increase of paracellular permeability induced by aloe-emodin-9-anthrone but did not completely reduce the concomitant increase in residual fluid volume. These findings suggest that aloe-emodin-9-anthrone has multiple mechanisms of action involved in the increase of water content in the rat large intestine.
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PMID:Studies of aloe. III. Mechanism of cathartic effect. (2). 215 53

Three newly detected dominant cataract mutations (Asc-1, Cat-3vao, Tcm) were investigated for effects on osmotic alterations in the lenses of heterozygotes. The lens wet weight was reduced in two mutant lines (Cat-3vao and Tcm), and the water content in the lenses of the Cat-3vao mice was increased. Moreover, in the cataractous lenses from Cat-3vao mice, the sodium-potassium-adenosine triphosphatase (Na(+)-K(+)-ATPase) activity was enhanced and the ATP concentration, correspondingly decreased. The osmotic variations observed in the Cat-3vao mutants might have been due to a metabolic response to the yet unknown, primary pathological event. The lenses of the other two mutant lines (Asc-1 and Tcm) revealed no alterations that could be related to osmotic stress. In no mutant line investigated could a decrease in Na(+)-K(+)-ATPase activity be demonstrated that was similar to the causative factor in the Nakano mutant line. The Cat-3vao mice exhibited some similarities to the Philly mutant line.
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PMID:Osmotic state of lenses in three dominant murine cataract mutants. 216 48

Aminoglycoside nephrotoxicity in experimental animals can be reduced by calcium loading, inducing diabetes, and giving thyroid hormone, while a potassium deficient diet enhances aminoglycoside nephrotoxicity. This study investigated whether potassium loading protects against gentamicin nephrotoxicity in the rat. In part I, group GK ate a diet containing 3.5% potassium and drank 0.2 mol/L KCl. Pair-fed rats eating a standard diet, group G, ate a 1% potassium diet and drank water. After 10 days, each group received gentamicin subcutaneously, 60 mg/kg twice daily for 8 days. The control groups, K and C, received the high or normal potassium diet, respectively. To control for a protective effect from a high solute load, the effect of equimolar NaCl loading was studied in group GNa and Na. At the end of the 8 days of gentamicin, inulin clearance was significantly higher in GK compared with G(0.6 +/- 0.1 v 0.3 +/- 0.1 mL/min per 100 g body weight [BW], P less than 0.05), but group GNa (0.4 +/- 0.1 mL/min per 100 g BW) was not different from group G. Morphological studies demonstrated that potassium-loaded rats (group GK) had significantly less proximal tubular necrosis compared with rats on a standard potassium diet, group G. Sodium loading did not protect against cellular necrosis. Part II studied renal function, cortical Na,K-adenosine triphosphatase (ATPase) and gentamicin accumulation after 2 days of gentamicin to determine the early functional and biochemical effects of potassium loading before overt renal functional impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of KCl loading in gentamicin nephrotoxicity. 216 23

A series of 4-substituted 8-[(2-benzimidazolyl)sulfinylmethyl]-1,2,3,4-tetrahydroquinolin es was synthesized and examined for their (H+ + K+)adenosine triphosphatase (ATPase)-inhibitory and antisecretory activities against histamine-induced gastric acid secretion in rats. Many compounds tested were potent inhibitors of (H+ + K+)ATPase. Most compounds showed antisecretory activity. The antiulcer activity against water-immersion stress-induced gastric ulcer, aspirin-induced gastric ulcer and gastric necrosis induced by hydrochloric acid also were tested in the rat. Some of these compounds, in particular, 4-(N-allyl-N-methylamino)-1-ethyl-8-[(5-fluoro-6-methoxy-2-benzimidazoly l) sulfinylmethyl]-1-ethyl-1,2,3,4-tetrahydroquinoline (XVIIx) were found to have potent activity. The structure-activity relationships are discussed.
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PMID:Synthesis and antiulcer activity of 4-substituted 8-[(2-benzimidazolyl)sulfinylmethyl]-1,2,3,4-tetrahydroquinoli nes and related compounds. 217 36

Our earlier studies of cataracts in Dahl salt-sensitive (DS) rats suggested the possibility of altered lens ion transport as a contributing factor in cataractogenesis in this genetic model. We also observed that those weanling DS rats with the greatest pressor response to a high salt diet eventually developed cataracts, and that changes in salt intake modified cataract formation. In the present studies, we measured lens 86Rb uptake as an index of sodium-potassium adenosine triphosphatase [(Na+,K+)-ATPase] activity in weanling DS rats before the development of cataracts or sustained hypertension. Additionally, plasma renin activity was measured to indirectly assess our hypothesis that the difference between cataract-prone DS rats and DS rats unlikely to develop cataracts might be a difference in degree of salt sensitivity. At the age of 4 weeks, 50 DS and 25 salt-resistant (DR) rats were given a high sodium diet for 2 weeks, at which time the rats were divided into three groups based on the systolic blood pressure response, that is, cataract-prone DS rats with systolic blood pressure equal to or greater than 155 mm Hg, DS rats unlikely to develop cataracts with systolic blood pressure less than or equal to 125 mm Hg, and DR rats. Lens and aqueous humor Na+ and K+, lens dry weight, and water content were not significantly different among the three groups of weanling rats. Plasma renin activity was lowest in cataract-prone DS rats and low in DS rats unlikely to develop cataracts when compared with values in DR rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lenticular rubidium uptake and plasma renin activity in weanling cataract-prone salt-sensitive rats. 240 57

The effect of concurrent low protein (8% casein) diet and lead (Pb) exposure (1 mg/ml lead acetate in drinking water) on testes of weaned rats up to 90 days of age was investigated Histopathological examination of testes of lead treated rats maintained on low protein diet revealed marked pathological changes associated with greatly reduced succinic dehydrogenase, glucose-6-phosphate dehydrogenase and adenosine triphosphatase activity as revealed histochemically compared to lead treated rats fed normal protein diet. It was concluded that higher accumulation of lead may be responsible for altering the enzyme levels and inducing the testicular degeneration to a greater extent in low protein fed rats compared to their counterpart controls.
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PMID:Lead induced testicular changes in protein malnourished rats. 250 Mar 71

Vanadate has been used in many cellular systems to elucidate mechanisms of enzyme action. Vanadate inhibits Na-K adenosine triphosphatase (ATPase) activity in many tissues. In isolated collecting tubule it inhibits sodium transport and vasopressin-stimulated water flux, the latter presumably distal to cyclic AMP formation. Depending upon the tissue studied, vanadate also stimulates a variety of cellular reactions including adenylate cyclase, glucose oxidation and glycogen synthesis. We studied the effect of varying concentrations of vanadate on N-ethylmaleimide (NEM)-sensitive ATPase activity in microdissected segments of rat nephron. In proximal convoluted tubule and in cortical, medullary and papillary collecting ducts vanadate had no effect on enzyme activity. In medullary and cortical thick ascending limbs, however, vanadate significantly stimulated NEM-sensitive ATPase activity (medullary thick ascending limb, 241 +/- 14 pmol/mm/hr vs. 531 +/- 74 pmol/mm/hr; control vs. (1 mM) vanadate, respectively; n = 14, P less than 0.01). The stimulatory effect of vanadate on NEM-sensitive ATPase activity was present at 5 microM vanadate, a concentration that inhibited Na-K ATPase activity approximately 80%. Metabolic acidosis also stimulated enzyme activity in the thick ascending limb, and the effect of vanadate was not additive. Metabolic alkalosis had no effect on NEM-sensitive ATPase in the thick ascending limb, but the stimulatory effect of vanadate was still seen. These data document that the NEM-sensitive ATPase in thick ascending limb is different from that found in other nonmammalian proton secretory epithelia which are vanadate inhibitable. The results with vanadate plus metabolic acidosis suggest that both are acting via the same mechanism.
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PMID:Vanadate stimulates the N-ethylmaleimide-sensitive adenosine triphosphatase in rat nephron. 252 98


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