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)

Cytosolic free sodium concentration ([Na+]i) and sodium transport systems were measured in intact platelets from 19 patients with early-stage chronic renal failure and 33 healthy control subjects using the novel fluorescent dye sodium-binding-benzofuran-isophthalate. Resting [Na+]i was significantly greater in patients with chronic renal failure compared to control subjects (40.8 +/- 3.1 mmol/l versus 32.2 +/- 2.0 mmol/l, mean +/- SEM, P < 0.05). After inhibition of Na-K-ATPase by 1 mmol/l ouabain a higher net sodium influx was observed in platelets from patients with chronic renal failure compared to control subjects (49.8 +/- 8.7 mmol/l versus 28.5 +/- 5.2 mmol/l, P < 0.05). The platelet Na-H exchanger was similar in the two groups. Cytosolic free calcium concentration ([Ca2+]i) was measured using fura2 and did not show significant differences between the two groups. To evaluate whether a circulating factor may be associated with elevated [Na+]i, a linked-enzyme Na-K-ATPase assay was included. Compared to control subjects plasma from patients with chronic renal failure produced a significant inhibition of steady-state Na-K-ATPase activity by 11.2 +/- 3.0% (P < 0.01). It is concluded that early-stage renal failure is associated with significant impairment of platelet sodium metabolism.
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PMID:Increased cytosolic free sodium in platelets from patients with early-stage chronic renal failure. 817 73

We have found abnormalities in Na-K-adenosine-triphosphatase (Na-K-ATPase) function in different tissues of rats with chronic renal failure (CRF). A potential mechanism for these findings is a change in Na-K-ATPase alpha- and/or beta-gene expression. To evaluate this possibility, we compared CRF with pair-fed, sham-operated rats to determine whether chronic uremia changes the expression of Na-K-ATPase alpha 1-, alpha 2-, beta 1-, and beta 2-isoform mRNAs or protein in different types of skeletal muscle, heart, liver, adipose, and kidney tissue. In CRF rats, alpha 1-mRNA in heart tended to be higher and beta 2-mRNA was lower in fat and kidney. There were no other statistically significant differences in isoform mRNAs in tissues of CRF compared with the control rats. Western blot analysis revealed a 38% increase in alpha 1-protein in adipocytes and a 61% decrease in kidney of CRF rats but no significant differences in the amounts of isoform protein in other tissues. Thus, in uremia, posttranslational events or inhibitors of the enzyme are more likely causes of defects in Na-K-ATPase than changes in mRNA or protein abundance.
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PMID:Na pump defects in chronic uremia cannot be attributed to changes in Na-K-ATPase mRNA or protein. 818 85

Chronic renal failure in the rat is associated with an impaired extrarenal potassium handling, whereas a renal adaptive mechanism of the remaining nephrons has been described. To understand the molecular basis of potassium homeostasis during renal failure we investigated the in vitro pump activity and the catalytic mRNA transcription in three different tissues: skeletal muscle, isolated adipocytes and kidney. The activity of the sodium pump, as measured by ouabain-sensitive 86Rb/K uptake in isolated adipocytes and skeletal muscle fibers, revealed a significant reduction of the pump activity in uremic rats. The reduction of the Na, K-ATPase activity in adipose tissue was associated with a similar decrement of both catalytic subunits (alpha 1 and alpha 2), whereas in the skeletal muscle tissue was only related to a decrease in the activity of the alpha 1 isoform. The expression of rat Na, K-ATPase catalytic isoforms mRNAs in kidney, muscle and adipose tissue from control and chronic renal failure rats was investigated at the molecular level with cDNA probes specific for the catalytic isoforms (alpha 1 and alpha 2). Northern blot analysis revealed that the respective catalytic mRNAs of uremic rats are regulated in a tissue-specific manner that are in agreement with the sodium-potassium pump activity. Muscle and adipose tissue showed a decrement in the levels of expression for the alpha 1 isoform mRNA. In contrast to these tissues, an increment in alpha 1 mRNA expression was observed in the kidney of rats with chronic renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue-specific modulation of Na, K-ATPase alpha-subunit gene expression in uremic rats. 819 69

1. We have studied Na+/K+ pump activity in vivo in three groups of subjects: patients with chronic renal failure not receiving maintenance dialysis, patients being treated by either haemodialysis or continuous ambulatory peritoneal dialysis, and matched control subjects. 2. To do this we have measured the changes in plasma and intraerythrocytic rubidium concentrations after an oral load of rubidium chloride, having previously shown that changes in the disposition of rubidium measured in this way reflect changes in the activity of the Na+/K+ pump in vivo. 3. Erythrocyte rubidium uptake was significantly reduced both in ten patients with chronic renal failure not receiving maintenance dialysis and in 12 patients being treated by haemodialysis, when compared with 31 healthy control subjects. In contrast, erythrocyte rubidium uptake was not altered in 13 patients treated by continuous ambulatory peritoneal dialysis. There was also a significantly reduced rate constant for erythrocyte rubidium uptake in patients with undialysed chronic renal failure (0.66 h-1) and in those treated by haemodialysis (0.78 h-1), whereas in patients treated by continuous ambulatory peritoneal dialysis the rate constant for erythrocyte rubidium uptake was not significantly different from control values (1.36 h-1 and 1.41 h-1, respectively). 4. These findings are consistent with a reversal of the inhibition of erythrocyte Na+/K+ pump activity in vivo found in chronic renal failure by continuous ambulatory peritoneal dialysis, but not by haemodialysis. This difference may be due to the failure of haemodialysis to clear a circulating inhibitor of Na+, K(+)-ATPase or to the rapid re-accumulation of such an inhibitor after haemodialysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of haemodialysis and continuous ambulatory peritoneal dialysis on abnormalities of ion transport in vivo in patients with chronic renal failure. 828 66

1. Uridine and uridine monophosphate (UMP) are natriuretic and a vasopressor in intact rats. In deoxycorticosterone acetate (DOCA)-salt hypertensive rats metabolic clearance rate (MCR) of uridine is raised and basal plasma uridine diminished, suggesting that metabolism of uridine is linked to changes in extracellular space. 2. Plasma uridine concentration was raised in 38 patients with chronic renal failure compared with age- and sex-matched healthy controls (8.49 mumol/L, 4.37-13.74 mumol/L median, interquartile range, and 2.64 mumol/L 2.51-2.74 mumol/L, respectively, P < 0.001). Plasma uridine was significantly diminished after isotonic fluid removal by ultrafiltration (UF) from 7.25 mumol/L (3.7-11.08) to 5.07 mumol/L (3.3-8.3), P < 0.001, whereas concentration of marker solutes urea and creatinine remained unchanged. During haemodialysis (HD), plasma uridine fell significantly from its pre-HD level. 3. In an animal model of expanded extracellular space the one-kidney, one-clip rat, plasma uridine was significantly higher (20.56 +/- 1.19 mumol/L, P < 0.01) and MCR diminished (34.93 +/- 3.44 mL/kg per min, P < 0.01) compared with sham-operated animals (plasma uridine 12.14 +/- 1.07 and MCR 53.59 +/- 4.11 mL/kg per min). Uridine or UMP did not inhibit Na+, K(+)-ATPase in either of the two assay systems. 4. It was concluded that catabolism of uridine is reduced by extracellular expansion and probably increased by volume reduction by UF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolism of uridine in expanded extracellular volume states. 839 45

Red blood cell (RBC) calcium level had been found to be higher in women than in men. This study was designed to evaluate whether this is a general phenomenon and to elucidate a possible mechanism for a gender-related difference in RBC calcium levels. Differences in RBC calcium levels between women and men were examined in normal subjects, in patients with chronic renal failure (CRF) who were known to have elevated RBC calcium levels, and in female and male rats. RBC calcium level was higher in healthy women (6.1 +/- 0.5 mumol/L in women vs 4.4 +/- 0.3 mumol/L in men; p < 0.01), in women with CRF (45.8 +/- 11.8 mumol/L vs 15.4 +/- 1.1 mumol/L in men with CRF; p < 0.025) and women undergoing hemodialysis treatment (43.4 +/- 4.7 mumol/L vs 8.8 +/- 0.9 mumol/L in men undergoing hemodialysis p < 0.001). RBC calcium levels in female rats were also significantly higher than those in male rats. Ovariectomy reduced RBC calcium levels in female rats to those of male rats, whereas castration of male rats had no effect on RBC calcium levels. These in vivo findings suggest that the elevated RBC calcium level is associated with activity of female sex hormones. To investigate a possible mechanism, the in vitro effect of beta-estradiol on calcium 45 influx into RBCs and its effect on basal and calmodulin-stimulated Ca adenosine triphosphatase (CaATPase) activity in RBC membranes was determined. CaATPase activity was not affected by beta-estradiol at various concentrations and different incubation periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Red blood cell calcium level is elevated in women: enhanced calcium influx by estrogens. 844 97

The aim of this study was to test basal and after treatment erythrocyte sodium and calcium concentrations, and calcium-ATPase activity and platelet cytosolic free calcium and pH in 20 normotensive controls, 20 hemodialysis-dependent chronic renal failure patients and in 18 essential hypertensives. Prior to treatment, essential hypertensive and uremic patients presented similar higher platelet calcium concentrations and lower pH than the normotensive control group. The erythrocyte sodium, calcium, and magnesium concentrations were only significantly elevated in chronic renal failure, with a significant decrease in the calcium-ATPase activity in the latter population. Hemodialysis partially reversed these intracellular ionic abnormalities with normalization of platelet pH. Significant correlations have been noted between weight loss and decreases in platelet calcium concentration (r = 0.60, p < 0.01) or in erythrocyte sodium (r = 0.50, p < 0.05). The systolic blood pressure decrease was only correlated to the increase in calcium-ATPase activity (r = 0.57, p < 0.05). Antihypertensive treatment (captopril and nifedipine) only tended to normalize the intracellular calcium concentration with correlation between the decrease of the latter and blood pressure decrease (r = 0.64 for the systolic blood pressure and 0.68 for the diastolic blood pressure, p < 0.01). Thus, in essential hypertension and in uremia, some cellular ionic abnormalities exist in platelets in baseline condition. Moreover, in uremia, erythrocyte presents abnormal ionic pattern. Some, but not all of these abnormalities could be corrected by treatment affecting blood pressure (cellular calcium) in essential hypertension or by hemodialysis (cellular sodium, calcium, and pH). In the latter treatment, the changes are linked to extracellular fluid modification. In essential hypertension, the intracellular calcium reduction was linked to blood pressure decrease.
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PMID:Intracellular cation concentrations in essential hypertension and chronic renal failure. 849 May 92

The results of the studies reported here demonstrate the cardiac non-haematopoietic effect of erythropoietin, providing a new physiological function of the hormone. We demonstrate that myocardium from rat with chronic renal failure (CRF) showed an abnormal response to ouabain associated with an inhibition of cardiac Na+/K+/ATPase activity and with a decrease in the high affinity 3H-ouabain binding sites. The extent to which both actions were improved with the recombinant human erythropoietin (rHuEpo) treatment suggests that the lack of the hormone is responsible for this phenomenon. The fact is that neither contractile nor enzymatic action of rHuEpo was accompanied with the improvement of the functional renal and haematologic parameters, indicating a primary effect on myocardial contractile function of rHuEpo, independent of the anaemic and uraemic state of the animal. The reason why erythropoietin is able to modulate directly the cardiac Na+/K+ pump makes it possible to conclude that the lack of erythropoietin in CRF may be at least in part responsible for the inhibition of cardiac enzymes, altering the contractile behaviour of the heart.
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PMID:Erythropoietin modified the cardiac action of ouabain in chronically anaemic-uraemic rats. 856 53

Compromised renal function predisposes to volume-dependent hypertension. Increased plasma levels of a sodium pump inhibitor as a possible pathogenetic factor have been demonstrated by many investigators in such patients, but efforts to identify the responsible agent have led to many, diverse candidates. Our premise in this study is that candidacy must depend on the satisfaction of rigorous criteria, including a specific action of the agent on the sodium pump. These criteria included reversibility, concentration dependence, receptor mediation, and an action at the appropriate step in the enzyme cycle. These criteria were applied to a potent [Na,K]ATPase inhibitor we have identified in the peritoneal dialysate of patients with chronic renal failure, present only during extracellular fluid volume expansion, the levels of which are correlated with the blood pressure rise that results from excessive NaCl and water intake. In microsomes that contained both [Na,K]ATPase and other ATPases, this candidate inhibited only the Na and K dependent, ouabain-sensitive ATPase. It displaced ouabain from the cardioglycoside binding site and its binding was linked to inhibition. Inhibition was produced by slowing the pump's dephosphorylation step, the exact action of all cardioglycosides. Finally, the candidate cross reacted with a digoxin Fab fragment and this Fab reversed its inhibition of [Na,K]ATPase. Together, these experiments demonstrate that the PD candidate specifically, and reversibly, inhibits the sodium pump via the cardioglycoside binding site, and hence, meets this crucial criterion for candidacy.
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PMID:Specificity of the volume-sensitive sodium pump inhibitor isolated from human peritoneal dialysate in chronic renal failure. 882 26

Few studies have examined tubular function after subtotal nephrectomy (Nx) and conservative treatments. The effects of 70% and 80% Nx (associated with dietary phosphate restriction in the latter case) on the apical brush border membrane (BBM) enzymes 5'-nucleotidase, gamma glutamyl-transferase and alkaline-phosphatase, and one BBM Na-phosphate cotransporter (NaPi-2) were studied in rats after a six week period. Changes in activity and mRNA abundance of the BBM enzymes and in NaPi-2 protein and mRNA abundance were compared with changes in the distal markers of Na,K-ATPase activity and epidermal growth factor (EGF) production. The activity, but not the mRNA of BBM enzymes, was moderately reduced by the 70% Nx. Both the mRNA and activity of gamma glutamyl-transferase and alkaline-phosphatase were decreased in the 80% Nx, and the NaPi-2 mRNA, protein and Na,K-ATPase activities were also reduced. These effects (except for 5'nucleotidase and Na,K-ATPase) were partly reversed by phosphate restriction. Overproduction of EGF occurred after the 70% Nx, was blunted in the 80% Nx, and then partially restored by phosphate restriction. Aggravation of tubular alteration was associated with enhanced renal hyperplasia (increased DNA mass), reduced GFR and hyperphosphatemia, and high PTH levels, but reduced cAMP excretion. Improvement following phosphate restriction was associated with reduced hyperplasia and lowering of phosphatemia and PTH levels. These data demonstrate that Nx selectively affected BBM function through transcriptional changes that were partially reversed by phosphate restriction. Regulatory factors involved in these changes may include intracellular phosphate content and growth factors, but not the PTH effects that are impaired in chronic renal failure.
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PMID:Subtotal nephrectomy alters tubular function: effect of phosphorus restriction. 940


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