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)

After 24-hr storage of canine kidneys with extracellular or intracellular (Ursol) solutions, the cortical and medullary renal ATPase enzymes (total Na+ + K+ and Mg-ATPase, Na+ + K+ -ATPase, and Mg-ATPase) were examined. It was found that storage with extracellular solution decreased all cortical enzymes. This was not the case with intracellular solution or in kidneys cooled and stored without any solution. A decrease in the potassium concentration of the Ursol solution decreased cortical (Na+ + K+)-ATPase enzymatic activity. The medullary enzymatic changes were similar in the different groups, and lower than in unstored controls. It appears that the changes on the level of the ATPase enzyme system which is related to the cation transport system might play a significant role in explaining the different results seen in clinical or experimental renal preservation systems. These changes can be related to the injury of preservation due to environmental effects of the cation concentrations and to a lesser degree to the damage of the enzyme system which provides the energy for cation transport.
Proc Eur Dial Transplant Assoc 1975
PMID:Changes of renal ATPase enzymes in different types of kidney preservation. 12

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.
Proc Clin Dial Transplant Forum 1977
PMID:Alternate reasons for atherogenesis in uremia. 15 May 96

In the present study 1 h of total occlusion of the left renal artery in conscious rats was chosen as experimental model of ischemic acute renal failure (ARF), while the contralateral kidney was left intact. Chronic high dietary sodium intake, acute isotonic saline infusion, or administration of saralasin did not protect from ARF. Furosemide, mannitol, and verapamil converted oliguric into non-oliguric ARF in 100%, 75%, and 60% of the animals, resp. Protection from oliguria and preservation of GFR inversely correlated with the depression of cortical ATP-concentration (control: 1.32 +/- 0.07 mumoles/g wet weight) 6 h after ischemia by 16%, 41%, and 58% in mannitol- and verapamil- treated rats and in untreated rats, resp. At this time, Na-K-ATPase enzyme activities in renal cortex and papilla were unaffected, while enzyme activity in outer medulla was suppressed from 15.4 +/- 1.4 to 9.4 +/- 1.0 mumoles Pi/mg protein h in all groups of animals. The results suggest that in this model of ARF renal ischemia not only affects cellular energy supply in renal cortex but also causes severe structural and functional impairment in the outer medulla, probably leading to tubular obstruction and depression of glomerular function. Pharmacological protection from ischemic oliguric ARF cannot be achieved by prior induction of high urine flow rates alone but depends on the degree of metabolic and functional reserve of the injured tubular epithelium.
Clin Exp Dial Apheresis 1983
PMID:Renal functional and metabolic studies on the role of preventive measures in experimental acute ischemic renal failure. 641

We examined the role of reactive oxygen metabolites and the protective effect of zinc-induced metallothionein (MT) synthesis on gentamicin nephrotoxicity both in vivo and in vitro. In vivo study we found that the MT content of renal cortex of the zinc preinjected rats was significantly increased, and proximal tubular necrosis and acute renal failure caused by injection of gentamicin were ameliorated. In suspended proximal tubules (PT), Na(+)-K(+)-ATPase activity and DNA synthesis were suppressed by the addition of gentamicin, but in zinc-pretreated rats' PT, these were not suppressed by the addition of gentamicin. Meanwhile MDA and hydroxyl radicals were significantly less in zinc-pretreated rats' PT compared to that in the control. Finally, we found that gentamicin enhanced superoxide anion and hydroxyl radical productin in renal cortical mitochondria. Superoxide anion could be suppressed by SOD and hydroxyl radical could be scavenged by DMSO, DFO and CAT. Our data confirm that hydroxyl radicals play a role in the pathogenesis of gentamicin nephrotoxicity, gentamicin can induce suppression of Na(+)-K(+)-ATPase activity and DNA synthesis in rats' proximal tubules leading to renal injury; this injury may be relevant to reactive oxygen metabolites generated by gentamicin. Renal cortical mitochondria is the source of reactive oxygen metabolites, which induces renal injury, and zinc-induced metallothionein synthesis could ameliorate gentamicin nephrotoxicity via scavenging reactive oxygen metabolites.
Nephrol Dial Transplant 1994
PMID:Mechanism of gentamicin nephrotoxicity in rats and the protective effect of zinc-induced metallothionein synthesis. 780 Feb 47

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.
Nephrol Dial Transplant 1994
PMID:Increased cytosolic free sodium in platelets from patients with early-stage chronic renal failure. 817 73

Several rat models of polycystic kidney disease (PKD) have been published. The only rat model of autosomal dominant polycystic kidney disease currently used is the so-called Hannover rat (Han:SPRD cy/+). This model is characterized by a slow progression of uraemia, proteinuria and hyperlipidaemia. Histological changes clearly resemble those seen is human PKD. The localization of Na+/K(+)-ATPase correlating with the phenotype of the cysts--basal in moderately expanded and apical in highly expanded cysts--suggests that the mislocation of the Na+/K(+)-ATPase is involved in the mechanism of cyst expansion rather than formation, and a consequence of cell dedifferentiation rather than an initial event. Of note is a considerable gender difference in disease severity. Disease anticipation or genetic imprinting does not occur. In addition to gender, a number of interventions influence the progression rate: acceleration is noted after unilateral nephrectomy, the induction of acidosis, chloride feeding or an increased protein intake; slowing down of the course occurs after the induction of alkalosis and castration, and after treatment with lovastatin and methylprednisolone. Thus the Han:SPRD cy/+ rat represents the only well-documented rat model of autosomal dominant PKD resembling a number of features of the human disease.
Nephrol Dial Transplant 1996
PMID:Rat models of autosomal dominant polycystic kidney disease. 904 28

Many vascular diseases in diabetes are known to be associated with the activation of the diacylglycerol (DAG)-protein kinase C (PKC) pathway. The major source of DAG that is elevated in diabetes is de novo synthesis from glycolytic intermediates. Among the various PKC isoforms, the beta-isoform has been shown to be persistently activated in diabetic animals. Multiple lines of evidence have shown that many vascular alterations in diabetes--such as a decrease in the activity of Na+-K+-adenosine triphosphatase (Na+-K+-ATPase), and increases in extracellular matrix, cytokines, permeability, contractility, and cell proliferation--are caused by activation of PKC. Inhibition of PKC by two different kinds of PKC inhibitors, LY333531, a selective PKC-beta-isoform inhibitor, and d-alpha-tocopherol, were able to prevent or reverse the various vascular dysfunctions in diabetic rats. These results have also provided in vivo evidence that DAG-PKC activation could be responsible for the hyperglycemia-induced vascular dysfunctions in diabetes. Clinical studies are now being performed to clarify the pathogenic roles of the DAG-PKC pathway in developing vascular complications in diabetic patients.
Perit Dial Int 1999
PMID:The role of protein kinase C activation in the pathogenesis of diabetic vascular complications. 1040 23

In the present study, the effect of potassium depletion on the expression of acid-base transporters in the collecting duct was examined. Toward this end rats were fed a potassium-free diet for 3 weeks. Thereafter, the expression of the basolateral chloride/bicarbonate exchangers AE1 and SLC26A7 and the apical H(+)-ATPase was examined by northern hybridization, immunoblot analysis and immunofluorescence labelling. The mRNA expression of AE1 increased by a robust approximately 500% in the cortex and approximately 70% in the outer medulla, which translated into a huge increase in AE1 protein abundance in the cortex and a moderate increase in the outer medulla in K-depletion. The mRNA expression of SLC26A7 did not change significantly but its protein abundance showed a robust increase in the outer medulla. The expression of SLC26A7 remained undetected in the cortex in K-depleted rats. The post translational increase in SLC26A7 membrane abundance in potassium depletion was recapitulated in vitro using epitope-tagged SLC26A7. H(+)-ATPase displayed enhanced apical plasma membrane immunoreactivity in the OMCD in K-depletion. We suggest that the up-regulation of SLC26A7 and AE1 on the basolateral membrane of A-intercalated cells in the OMCD and CCD, respectively, along with H(+)-ATPase on the apical membrane, contributes to enhanced bicarbonate absorption in the collecting duct in K-depletion.
Nephrol Dial Transplant 2007 Dec
PMID:Regulation of the basolateral chloride/base exchangers AE1 and SLC26A7 in the kidney collecting duct in potassium depletion. 1780 57

The permeability for small solutes and the ultrafiltration capacity of the peritoneum are essential for effective peritoneal dialysis (PD) treatment. Elucidation of the factors that regulate these two properties is therefore of great importance. Ouabain, a potent inhibitor of the Na+-K+ pump has been shown to reduce fluid absorption in animal models of PD. In the present study, we used Ussing chamber experiments to investigate the effect of ouabain on the transmesothelial electrical resistance (RTM) of isolated visceral sheep peritoneum. Peritoneal samples from the omentum of adult sheep were isolated immediately after the deaths of the animals and were transferred to the laboratory in cooled Krebs-Ringer bicarbonate solution (4 degrees C, pH 7.5) bubbled with 95% O2/5% CO2. A planar sheet of visceral peritoneum was mounted in an Ussing-type chamber, and ouabain (10(-3) mol/L) was added apically and basolaterally. The RTM was measured before and serially for 30 minutes after the addition of ouabain. Because active ion transport is temperature-dependent, all measurements were taken at 37 degrees C. The results presented are the mean +/- standard error of 6 experiments. Before the addition of ouabain, the control RTM was measured as 21.26 +/- 0.57 Omega x cm2. Addition of ouabain basolaterally induced an increase in the RTM to 27.62 +/- 0.72 Omega x cm2 within 1 minute (p < 0.05), and this level persisted throughout the experiment. The effect of ouabain, when added apically, was similar, characterized by a rapid rise in the RTM to 24.66 +/- 0. 76 Omega x cm2 at 1 minute (p < 0. 05), with subsequent persistence at that level. A clear association between RTM and active ion transport has been shown in previous studies. The results of the present study, showing a rapid effect of ouabain on the RTM of visceral peritoneum, therefore clearly suggest that cell membrane Na+K+-ATPase is important for peritoneal ionic transport. In addition, ouabain was previously shown to reduce vasodilation and intraperitoneal sodium or to increase intraperitoneal volume, especially in the presence of conventional acidic solutions. Those findings, combined with the results of the present study, clearly indicate that intraperitoneal administration of digitalis glycosides may have some beneficial effect in PD patients; however the specific clinical implications need further investigation.
Adv Perit Dial 2007
PMID:Effect of sodium-potassium pump inhibition by ouabain on the permeability of isolated visceral sheep peritoneum. 1788 1

The objective of this study was to identify the cardiodepressant autoantibodies that could directly influence left ventricular ejection fraction (LVEF) in patients with dilated cardiomyopathy (DCM), as well as to establish a simple screening method for these antibodies. Not only acute hemodynamic but also chronic prognosis improvements were reported with immunoadsorption in some patients with DCM. Various antibodies determined by immunohistochemistry, immunoblotting, and enzyme-linked immunosorbent assay (beta1-adrenergic [beta1-] receptors, muscarinic M2-acetylcholine [M2-] receptors, troponin I, or Na-K-ATPase) were measured in 104 patients with DCM. Cardiodepressant antibodies were also determined by ultrasonic echocardiography (UCG) of 18 day old chick embryos after adding the patients' purified immunoglobulin G, and the following clinical features were compared: age, gender, New York Heart Association class, LVEF, neurohumoral factors, arrhythmias, and other antibodies. We also checked the in vitro immunoadsorption effect against these cardiodepressant antibodies. Cardiodepressant antibodies were found in 63% of 104 patients with DCM and had no relation to other clinical parameters, except for some antibodies such as anti-beta1-receptor antibodies (81% vs. 52%, P < 0.01), anti-M2-receptor antibodies (83% vs. 48%, P < 0.01), or anti-Na-K-ATPase antibodies (85% vs. 55%, P < 0.01). However, cardiodepressant antibodies were similarly found in patients with and without antibodies against troponin I (56% vs. 64%). The LVEF of chick embryos measured by UCG in the presence of patient serum was improved after in vitro immunoadsorption. The ex vivo system using chick embryos was able to determine cardiodepressant antibodies. By multivariate analysis, antibodies against beta1- or M2-receptors was a predictor of these autoantibodies.
Ther Apher Dial 2008 Apr
PMID:Autoantigen estimation and simple screening assay against cardiodepressant autoantibodies in patients with dilated cardiomyopathy. 1838 58


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