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)

Red blood cells from 7 out of 13 patients with chronic uremia were found to have increased intracellular concentrations of sodium associated with a reversible inhibition of ouabain-sensitive Na efflux when incubated in control plasma. Although mean Na-K-ATPase activity of RBC hemolysates was only moderately decreased (21.8 +/- 1.5 vs. 26.5 +/- 1.8 nmol Pi/mg protein/h), enzyme kinetics revealed a significant increase in KmATP values for this enzyme in uremic RBCs (1.01 +/- 0.1 vs. 0.58 +/- 0.03; p less than 0.001) which was closely correlated to serum creatinine concentration (r = 0.9034). While aerobic glycolysis was unaltered, an increase in glucose-6-phosphate dehydrogenase activity was observed, i.e. the enzyme initiating the pentose-phosphate cycle. In addition, intracellular ATP concentrations of uremic RBCs were significantly higher than ATP concentrations of control RBCs (2.13 +/- 0.22 vs. 1.32 +/- 0.06 mmol/l RBC; p less than 0.01). These data suggest that high intracellular concentrations of Na and ATP in uremic RBCs partially result from a competitive reversible inhibition of the transport ATPase by uremic toxins.
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PMID:Functional and metabolic studies on red blood cell sodium transport in chronic uremia. 13 Dec 54

Subcellular fractions in hearts from rats with severe acute uremia (24 hours after total nephrectomy) and moderate chronic uremia (2 weeks after five sixths nephrectomy) were studied and compared with preparations from acute and chronic sham-operated rats, respectively. Calcium- and magnesium-sensitive actomyosin adenosine triphosphatase (ATPase) activities were normal in both groups. Acute uremia was associated with a significant depression of sarcolemmal Na+,K+ ATPase activity. Calcium transport by fragmented sarcoplasmic reticulum was also depressed in the presence and absence of oxalate in acute uremia. Mitochondrial calcium transport and adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were normal in these animals. Chronic uremic animals showed no abnormal subcellular mechanisms. These data suggest a direct effect of acute uremia on some membrane functions in myocardial cells. The discrepancies observed between acute and chronic uremic groups may be due to a different degree of uremic state. The observation of depressed calcium transport by fragmented sarcoplasmic reticulum (FSR) in acute uremic hearts which were previously shown to have increased contractile reserve suggests that studies of calcium transport in FSR may not always truly reflect the contractile capacity of the heart.
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PMID:Studies of subcellular control factors in hearts of uremic rats. 13 36

Uremia was induced in rats and rabbits by unilateral nephrectomy and partial resection of the contralateral kidney. The effectiveness of the procedure was checked by determining serum urea levels that 7 days after operation were found to be more than twice as high in the operated than in the sham operated animals. Serum electrolytes at this time did not show significant alterations. In the cardiac sarcolemma from both kinds of animals the specific (Na+,K+)-ATPase activity was significantly decreased in the uremic animals. The basic, Mg2+-dependent ATPase was not affected.
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PMID:Transport ATPases of cardiac sarcolemma in experimental uremia. 13 89

The key to symptomatology in uremia is nitrogen retention leading to amidination and transmidination of a variety of substrates. The product of this activity is a series of guanidino acids which are methyl receptors converting S-adenosylmethionine to adenosine and homocysteine. Adenosine is a potent inhibitor of the enzyme ATPase and, in this way, contributes to the anemia, the bleeding diathesis and the CNS symptoms of uremia. Homocysteine is an inhibitor of pyridoxal phosphate-induced reactions and contributes to the angiitis and thromboembolism so unexpectedly encountered in chronic uremia.
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PMID:Alternate reasons for atherogenesis in uremia. 15 May 96

Unilateral nephrectomy and partial resection of the contralateral kidney in rats causes uremia that lasts for several weeks and influenced overall (Na+, K+)-ATPase activity as well as p-nitrophenyl phosphatase (p-NPPase) in the plasma membranes of erythrocytes and heart. Both enzymatic activities are inhibited to a similar extent in the uremic animals, regardless of whether the membranes were investigated one or four weeks after surgical treatment.
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PMID:The effect of experimental uremia on potassium-activated phosphatase from erythrocyte and cardiac membranes. 20 79

Na-K-ATPase activity and renal function were compared in rats studied after relief of 24 h of unilateral or bilateral ureteral ligation (UUL or BUL), that is, in the absence or presence of post-obstructive diuresis. Na-K-ATPase activity in the outer medulla of the rat kidney after relief of UUL was not significantly altered immediately but was markedly reduced 1 and 3 days post-obstruction. The decrease in medullary Na-K-ATPase activity was not significantly different from that observed after relief of BUL. These results indicate that decreased Na-K-ATPase activity in the post-obstructive kidney is not responsible for post-obstructive diuresis and is not due to uremia, but is a local phenomenon which is probably secondary to altered renal structure or function. It may be due to decreased filtered sodium load or direct tubular damage, but other data suggests that the decreased medullary solute concentration gradient in the post-obstructive kidney (UUL or BUL) may influence Na-K-ATPase activity which, in turn, contributes to the decreased ability to conserve sodium and water.
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PMID:Post-obstructive nephropathy in the rat: relationship between NA-K-ATPase activity and renal function. 21 25

Arginase activity of erythrocyte membrane fragments has been determined in normal subjects and in two groups of uremic patients: 1) those having a blood urea concentration of 100 mgm/100 ml or higher and with an elevated erythrocyte sodium concentration and 2) patients with a blood urea concentration of 100 mgm/100 ml and higher and a normal erythrocyte sodium concentration. No statistically significant difference was detected between the normal subjects and the uremic patients. It is concluded, therefore, that the effect of uremia on the magnesium dependant, Na and K activated adenosine triphosphatase of erythrocyte membranes is not applicable to all enzymes of the erythrocyte.
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PMID:Arginase activity of human erythrocyte ghosts in uremia. 123 23

1. Calcium concentration and Ca(2+)-ATPase activity under basal conditions and after maximal stimulation with calmodulin were measured in erythrocytes from 32 patients with end-stage renal failure on haemodialysis and from 27 healthy subjects. 2. In patients with renal failure the Ca2+ concentration in erythrocytes was elevated compared with healthy subjects (4.27 +/- 1.02 versus 2.86 +/- 0.57 mumol/l, P less than 0.05). 3. Basal Ca(2+)-ATPase activity was lower in the patients with renal failure than in healthy subjects (4.62 +/- 1.34 versus 5.43 +/- 1.23 pmol of phosphate min-1 10(-6) erythrocytes). After maximal stimulation, Ca(2+)-ATPase activity reached 6.93 +/- 2.81 pmol of phosphate min-1 10(-6) erythrocytes in the patients with renal failure, whereas in healthy subjects stimulation yielded a Ca(2+)-ATPase activity of 32.54 +/- 8.48 pmol of phosphate min-1 10(-6) erythrocytes. 4. Incubation of erythrocytes from healthy subjects with plasma from uraemic patients caused inhibition of Ca(2+)-ATPase. Likewise, the ultrafiltrate from plasma obtained by haemofiltration treatment inhibited Ca(2+)-ATPase. 5. Gel chromatography of the ultrafiltrate and laser desorption/ionization mass spectroscopy revealed that a fraction containing substances with a molecular mass of about 300 Da inhibited Ca(2+)-ATPase. 6. It is concluded that, in uraemia, a Ca(2+)-ATPase inhibitor accumulates in the plasma, and this could contribute to the toxicity of uraemia by inhibiting cellular Ca2+ transport in erythrocytes and possibly other tissues.
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PMID:Isolation of an ultrafilterable Ca(2+)-ATPase inhibitor from the plasma of uraemic patients. 132 May 46

Ultrafiltrate obtained by hemodialysis of patients with uremia who were not taking cardiac glycosides was used as a source of Na, K adenosine triphosphatase inhibitor for purification and further study. Inhibitory activity was measured by a linked-enzyme assay and by effect on rubidium 86 uptake in guinea pig aortic strips. Two approaches were used in purification: dialysis with a 500 dalton membrane followed by gel filtration with Sephadex G-25, and removal of protein by acidification and boiling followed by Sephadex G-10. The first procedure failed to separate the inhibitor from the salt fraction, whereas the second separated the inhibitor from the salt peak but resulted in partial coelution of the inhibitor with endogenous pyruvate, which interferes with the linked-enzyme assay. Pooled, concentrated G-10 elution fractions from the early part of the inhibitor peak, which were free of pyruvate, produced a dose-response relationship by enzymatic assay that was close to parallel with that for ouabain. Like ouabain, these fractions also inhibited 86Rb uptake in guinea pig aorta. Despite these properties, our previous work has demonstrated that the inhibitor, unlike some other ouabain-like or digitalis-like substances obtained from blood or urine, has no apparent role in body fluid homeostasis.
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PMID:An Na, K ATPase inhibitor from ultrafiltrate obtained by hemodialysis of patients with uremia. 132 35

Previous studies have suggested that an alteration in the expression of the Na,K-ATPase of muscle may be an important determinant of enhanced insulin sensitivity in chronic renal failure. Therefore, in the present studies we have examined the effect of uremia on the Na,K-ATPase alpha isoforms in skeletal muscle, at the level of mRNA expression and enzymatic activity. The activity of the sodium pump, as measured ouabain-sensitive 86Rb/K uptake in soleus muscle, revealed a reduction in the activity in uremia, related to the increment in plasma creatinine values. The decrement in 86Rb uptake by the rat soleus muscle of experimental animals was associated with changes on Na,K-ATPase gene product. Northern analysis of mRNA revealed isoform-specific regulation of Na,K-ATPase by uremia in skeletal muscle: a decrease of approximately 50% in alpha 1 subunit Na,K-ATPase mRNA, as compared to controls. The decrement in alpha 1 mRNA correlates with the decreased activity of the Na,K-ATPase in uremia, under basal conditions and with the almost complete inhibition of the Na,K-ATPase, of uremic tissue by a concentration of 10(-5) M ouabain. Although the activity of the alpha 2 isoform pump was not modified by uremia, the 3.4-kb message for this enzyme was increased 2.2-fold; this discrepancy is discussed. Altogether these findings demonstrate that the defective extrarenal potassium handling in uremia is at least dependent in the expression of alpha 1 subunit of the Na,K-ATPase.
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PMID:Effect of chronic renal failure on Na,K-ATPase alpha 1 and alpha 2 mRNA transcription in rat skeletal muscle. 166


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