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)

The acceptance of a syndrome as a distinct nosological entity depends upon our ability to demonstrate that it consistent genetic, pathological and biochemical abnormalities. During the past two decades the application of enzyme histochemistry and electronmicroscopy to the study of biopsy muscle from patients from a variety of ill-defined neuromuscular disorders has enabled us to classify them with much greater precision. This approach, together with increasingly sophisticated electrophysiological techniques, has lead to a much clearer separation of neurogenic and primarily myopathic disorders with a consequent shrinkage in the category of pure muscular dystrophy. Perhaps the most useful application of morphological techniques alone has been in the field of congenital and metabolic myopathies, the histochemical and ultrastructural abnormalities in some cases providing valuable clues to the pathogenesis or even the aetiology of the underlying disease process. This applies particularly to the various glycogen storage diseases affecting skeletal muscle, disorders in which there appear to be structural and functional abnormalities of muscle mitochondria or in which excessive amounts of lipid are stored in muscle fibres. In this communication the histochemical and ultrastructural characteristics of these diseases will be detailed, their possible significance discussed and the relative non-specificity of some of these morphological abnormalities will be noted. A comment will be made on the frequency with which simple Type II fibre atrophy (as demonstrated by the myofibrillar ATPase preparation) may be accompanied by gross and bizarre ultrastructural abnormalities, e.g. in the myopathy accompanying chronic renal failure. Such inconsistencies underline the fact that it is not always possible to demonstrate a close correlation between histochemical and ultrastructural abnormalities in muscle disease. However, it should be emphasized that the combined approach is essential to the rational morphological study of these disorders.
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PMID:Correlations between histochemical and ultrastructural studies of diseased muscle. 123 67

The activity of Na(+)-K+ ATPase of pancreatic islets modulates their insulin secretion. The study presented here examined the activity of this enzyme in pancreatic islets of chronic renal failure (CRF) rats in an effort to further delineate the mechanisms of impaired insulin secretion in CRF. The Vmax of Na(+)-K+ ATPase, but not its Km, and the ATP content are significantly reduced in islets of CRF rats that have elevated levels of parathyroid hormone (PTH). These derangements are prevented by prior parathyroidectomy of CRF rats (low blood levels of PTH) or by their treatment with the calcium channel blocker verapamil; these latter rats have sustained elevation of blood levels of PTH. The data indicate that the chronic excess blood levels of PTH in CRF initiates events (augmented entry of calcium) that lead to the reduction in ATP content and in Vmax of Na(+)-K+ ATPase of pancreatic islets. Reducing the blood levels of PTH by parathyroidectomy or blocking the action of PTH on calcium entry into cells by verapamil prevents these derangements. The results suggest that chronic inhibition of Na(+)-K+ ATPase may participate in the processes underlying the impaired insulin secretion in CRF.
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PMID:Reduced activity of Na(+)-K+ ATPase of pancreatic islets in chronic renal failure: role of secondary hyperparathyroidism. 132 Sep 48

This study was undertaken to evaluate the effect of chronic renal failure as well as dialysate sodium concentration during haemodialysis on membrane ATPase activity and erythrocyte sodium and potassium concentration. Intracellular Na and K were not changed in patients when compared to normal subjects. There was, however, a significant decrease of Na-K-ATPase activity in patients versus controls. Erythrocyte sodium increased during haemodialysis with low and normal sodium dialysate. The present results suggest that sodium dialysate concentration has an influence on the intracellular cationic homeostasis.
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PMID:Membrane ATPase, erythrocyte sodium and potassium in haemodialysis patients. 165 74

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

A study was made of the activity of Na, K-ATPase of red blood cells in children with chronic renal failure (CRF) before and after the treatment with hemodialysis. It has been discovered that in CRF children, the activity of Na, K-ATPase was significantly reduced as compared to that in the controls. Meanwhile after the dialysis therapy it rose, which may be due to the improvement of the work of Na, K-ATPase in the red blood cell membrane. It is suggested that the decline of the activity of Na, K-ATPase in CRF patients is likely to be related to the inhibition of the enzyme by digoxin-like factor. Based on an analysis of the data obtained it is recommended that, Na, K-ATPase be used as an effective criterion for estimation of the treatment adequacy or delineation of indications for hemodialysis in children suffering from CRF.
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PMID:[Effect of hemodialysis on the erythrocyte sodium, potassium adenosine triphosphatase activity in children with chronic renal failure]. 166 99

Glucose-induced insulin secretion is impaired in rats with chronic renal failure (CRF), and this defect is due to PTH-induced derangement in the metabolism of pancreatic islets, including an elevated basal level of intracellular calcium, low basal ATP content, low glucose-stimulated ATP and ATP/ADP ratio, and decreased maximum velocity of Ca(2+)-ATPase. Chronic treatment of CRF rats with verapamil prevented the impairment of insulin secretion. The present study examined the mechanism through which verapamil exerts this action. CRF rats treated with verapamil had high levels of serum PTH, but normal basal ATP content, a greater rise in ATP and ATP/ADP ratio after exposure to glucose, normal intracellular calcium and higher maximum velocity of Ca(2+)-ATPase. The results demonstrate that treatment of CRF rats with verapamil was associated with marked improvement or normalization of the CRF-induced metabolic derangements in pancreatic islets despite no effect on the serum level of PTH. The data are consistent with the notion that verapamil prevents the derangements in insulin secretion in CRF rats by blocking the action of PTH on the islets.
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PMID:Verapamil prevents the metabolic and functional derangements in pancreatic islets of chronic renal failure rats. 183 76

Chronic renal failure (CRF) is associated with a sustained rise in the concentration of cytosolic calcium [( Ca2+]i) of brain synaptosomes. This was attributed to secondary hyperparathyroidism where the excess blood levels of parathyroid hormone (PTH) augment calcium entry into synaptosomes. However, for such an effect of PTH to cause a sustained rise in [Ca2+]i, calcium extrusion out of synaptosomes should be impaired. The study presented here examined the effect of CRF with and without (CRF-PTX) excess PTH and the treatment of CRF rats with verapamil (V) on the Vmax and Km for calcium of synaptosomal Ca2+ ATPase, an enzyme that plays an important role in pumping calcium out of the synaptosomes. The Vmax of synaptosomal Ca2+ ATPase in CRF rats was significantly (P less than 0.01) lower than that of normal, CRF-PTX, CRF-V, and normal-V rats. However, the values in CRF-V were still below normal (P less than 0.05). There were no significant differences in the Km for calcium of synaptosomal Ca2+ ATPase among the five groups of animals. [Ca2+]i was significantly (P less than 0.01) higher in synaptosomes of CRF rats than in normal, CRF-PTX, CRF-V, and normal-V animals, and the values among the latter four groups were not different. The data demonstrate that the activity of synaptosomal Ca2+ ATPase is reduced in CRF rats, and this derangement is related to the excess PTH. This derangement in Ca2+ ATPase activity plays an important role in the genesis of the sustained elevation of synaptosomal [Ca2+]i in CRF.
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PMID:Effect of chronic renal failure on Ca2+ ATPase of brain synaptosomes. 183 13

It has been suggested that a sustained rise in resting levels of cytosolic calcium [Ca2+]i of pancreatic islets is responsible for impaired insulin secretion in chronic renal failure (CRF). Evidence for such an event is lacking and the mechanisms through which it may affect insulin secretion are not known. Studies were conducted in normal, CRF, and normocalcemic, parathyroidectomized (PTX) CRF rats to answer these questions. Resting levels of [Ca2+]i of islets from CRF rats were higher (P less than 0.01) than in control of CRF-PTX rats. [3H]2-deoxyglucose uptake and cAMP production by islets were not different in the three groups. Insulin content of, and glucose-induced insulin secretion by islets from CRF rats was lower (P less than 0.01) than in control and CRF-PTX rats. In contrast, glyceraldehyde-induced insulin release by CRF islets was normal. Basal ATP content, both glucose-stimulated ATP content and ATP/ADP ratio, net lactic acid output, Vmax of phosphofructokinase-1, and Ca2+ ATPase of islets from CRF rats were lower (P less than 0.02-less than 0.01) than in normal or CRF-PTX animals. Data show that: (a) Glucose but not glyceraldehyde-induced insulin secretion is impaired in CRF; (b) the impairment in glucose-induced insulin release in CRF is due to a defect in the metabolism of glucose; (c) this latter defect is due to reduced ATP content induced partly by high [Ca2+]i of islets; and (d) the high [Ca2+]i in islets of CRF rats is due to augmented PTH-induced calcium entry into cells and decreased calcium extrusion from the islets secondary to reduced activity of the Ca2+ ATPase.
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PMID:On the mechanism of impaired insulin secretion in chronic renal failure. 198 99

Red blood cell (RBC) calcium, calcium 45 influx, and calcium extrusion as indicated by Ca-stimulated, Mg-dependent adenosine triphosphatase (CaATPase) was determined in patients with chronic renal failure (CRF), patients with CRF receiving continuous ambulatory peritoneal dialysis (CAPD) treatment, and controls. Cell calcium, which in the controls was 5.5 mumol/L of cells, was elevated in patients with CRF--30.6 +/- 6.8 mumol/L of cells (p less than 0.002)--and in patients receiving CAPD-23.6 +/- 6.7 mumol/L of cells (p less than 0.02). Basal CaATPase activity in controls was 850.7 +/- 66.7 nmol inorganic phosphate per milligram of protein per hour. It was suppressed in patients with CRF and patients receiving CAPD: 504.9 +/- 34.4 nmol inorganic phosphate per milligram of protein per hour and 618.2 +/- 47.3 nmol inorganic phosphate per milligram of protein per hour, respectively (p less than 0.01). Calmodulin-stimulated CaATPase revealed a pattern similar to that of CaATPase basal activity. RBC calcium showed an inverse correlation with CaATPase activity (r = -0.935, p less than 0.005) in patients with CRF. Calcium influx was increased in patients with CRF and in patients receiving CAPD: 12.00 +/- 1.34 mumol/L of cells per hour and 13.60 +/- 1.70, respectively, compared with 4.61 +/- 0.39 mumol/L of cells per hour in controls (p less than 0.001). Patients with CRF have elevated RBC calcium levels mainly related to decreased extrusion and to increased influx. CAPD fails to improve substantially these abnormalities. Plasma vanadium levels were markedly elevated in patients undergoing hemodialysis and marginally in patients receiving CAPD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Red blood cell calcium level in chronic renal failure: effect of continuous ambulatory peritoneal dialysis. 214 69

Diabetics have an increased risk of developing renal insufficiency, as well as congestive heart failure independent of coronary atherosclerotic or hypertensive heart disease. Aluminum toxicity is being recognized with increased frequency in patients with reduced renal function and aluminum accumulates to a greater degree in tissues of patients with diabetes. Studies in patients with end stage renal disease have implicated aluminum overload as a potential cause of reduced cardiac function. Since both diabetes and aluminum decrease the activity of (Ca + Mg)-ATPase, a key enzyme involved in myocardial calcium transport, the interaction of experimental diabetes mellitus and aluminum toxicity on myocardial sarcoplasmic reticulum calcium transport was investigated in rats. Aluminum alone had no effect on (Ca + Mg)-ATPase activity, while activities in both the diabetic ([DM]) and diabetic plus aluminum loaded ([DM + Al]) groups were significantly lower than controls ([C]). Oxalate-dependent calcium uptake in the [DM] rats was slightly, but not significantly lower than controls, however, uptake was markedly reduced in rats which were both diabetic and aluminum loaded. The calcium regulatory protein calmodulin was measured by a functional assay in the soluble fraction of myocardial tissue prepared from each of the four groups. Compared to [C], calmodulin activity was significantly reduced in both the [DM] and [DM + Al] groups but not affected by aluminum alone. These data indicate that diabetes mellitus is associated with decreased myocardial calmodulin activity that may contribute to reduced sarcoplasmic reticulum (Ca + Mg)-ATPase and calcium transport activities and that aluminium toxicity potentiates the adverse effects of diabetes on decreasing sarcoplasmic reticulum calcium uptake.
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PMID:Effects of diabetes mellitus and aluminum toxicity on myocardial calcium transport. 214 51


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