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 progress of chronic renal failure (CRF) is characterized by the development of glomerular and tubular lesions. However, little is known about the expression of organic anions renal transporters. The objective of this work was to study, in rats with experimental CRF (5/6 nephrectomy), the expression of the organic anion transporter 1 (OAT1) and organic anion transporter 3 (OAT3) and their contribution to the pharmacokinetics and renal excretion of p-aminohippurate (PAH). Two groups of animals were used: Sham and CRF. Six months after surgery, systolic blood pressure and plasma creatinine concentrations were significantly higher in CRF groups. CRF rats showed a diminution in: the filtered, secreted and excreted load of PAH; the systemic clearance of PAH; the renal OAT1 expression; and the renal Na-K-ATPase activity. No remarkable modifications were observed in the OAT3 expression from CRF kidneys. The diminution in the systemic depuration and renal excretion of PAH may be explained by the decrease in its filtered and secreted load. The lower OAT1 expression in remnant renal mass of CRF rats or/and the lower activity of Na-K-ATPase might justify, at least in part, the diminished secreted load of this organic anion.
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PMID:Altered renal elimination of organic anions in rats with chronic renal failure. 1587 38

Hyperleptinemia may be involved in the pathogenesis of obesity-associated hypertension, however, the mechanism of hypertensive effect of leptin is incompletely elucidated. Previously, we have demonstrated that chronic hyperleptinemia causes up-regulation of renal Na+,K+-ATPase and decreases urinary Na+ excretion. Herein, we investigated whether antioxidant treatment could correct these abnormalities. The study was performed on male Wistar rats. Leptin administered for 7 days (0.25 mg/kg twice daily sc) increased systolic blood pressure by 20.6%. Leptin had no effect on urine output and creatinine clearance but reduced sodium excretion by 40.1%. Na+,K+-ATPase activity in the renal cortex and medulla was higher in leptin-treated rats by 24.3% and 80.6%, respectively. In addition, hyperleptinemia was associated with an increase in plasma and urinary 8-isoprostanes and reduced urinary excretion of nitric oxide (NO) metabolites and cGMP. Co-treatment with a superoxide dismutase mimetic, tempol, or an NAD(P)H oxidase inhibitor, apocynin (2 mM in the drinking water), prevented leptin-induced blood pressure elevation, normalized plasma and urinary 8-isoprostanes, urinary excretion of sodium, NO metabolites and cGMP, as well as prevented up-regulation of renal Na+,K+-ATPase activity. These data suggest that hyperleptinemia increases renal Na+,K+-ATPase activity and reduces natriuresis by inducing oxidative stress-dependent NO deficiency. Antioxidant treatment is effective in leptin-induced hypertension and should be considered in controlling blood pressure in hyperleptinemic obese individuals.
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PMID:Antioxidant treatment normalizes renal Na+,K+-ATPase activity in leptin-treated rats. 1588 21

The present study was designed to examine whether aqueous extract of steamed root of Rehmannia glutinose (ARR) has an ameliorative effect on renal functional parameters in association with the expressions of aquaporin 2 (AQP 2), Na,K-ATPase, and heme oxygenase-1 (HO-1) in the ischemia-reperfusion induced acute renal failure (ARF) rats. Polyuria caused by down-regulation of renal AQP 2 in the ischemia-induced ARF rats was markedly restored by administration of ARR (200 mg/kg, p.o.) with restoring expression of AQP 2 in the kidney. The expressions of Na,K-ATPase alpha1 and beta1 subunits in the renal medullar and cortex of the ARF rats were also restored in the ARF rats by administration of ARR. On the other hand, administration of ARR lowered the renal expression of HO-1 up-regulated in rats with ischemia-induced ARF. The renal functional parameters including creatinine clearance, urinary sodium excretion, urinary osmolality, and solute-free reabsorption were also markedly restored in ischemia-ARF rats by administration of ARR. Taken together, these data indicate that RSR ameliorates renal defects in rats with ischemia-induced ARF.
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PMID:Rehmannia glutinose ameliorates renal function in the ischemia/reperfusion-induced acute renal failure rats. 1614 36

The present study was designed to examine whether Yukmijihwang-tang (YJT), which is a Korean decoction for the treatment of renal disease, has an effect on renal functional parameters in association with the expression of aquaporin 2 (AQP 2), Na,K-ATPase, heme oxygenase-1 (HO-1) in rats with ischemia/reperfusion-induced acute renal failure (ARF). Polyuria caused by down-regulation of renal AQP 2 in the ischemia/reperfusion-induced ARF rats was markedly restored by administration of YJT (100 or 200 mg/kg, p.o.) with restoring expression of AQP 2 in the kidney. The expressions of Na,K-ATPase alpha1 and beta1 subunits in the renal medulla and cortex of the ARF rats were also restored in them by the administration of YJT. Administration of YJT lowered the expression of renal HO-1, which was up-regulated in rats with ischemia/reperfusion-induced ARF. The renal functional parameters including creatinine clearance, urinary sodium excretion, urinary osmolality, and solute-free reabsorption were also markedly restored in ischemia-ARF rats by administration of YJT. Histological study also showed that renal damages in the ARF rats were abrogated by administration of YJT. Taken together, these data indicate that YJT ameliorates renal defects in rats with ischemia/reperfusion-induced ARF.
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PMID:Yukmijihwang-tang ameliorates ischemia/reperfusion-induced renal injury in rats. 1618 23

The present study was done to determine whether endogenous nitric oxide (NO) plays a role in the regulation of sodium transporters in the kidney. Male Sprague-Dawley rats were treated with NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/L drinking water) for 4 weeks. Control rats were supplied with tap water without drugs. Expression of Na, K-ATPase, type 3 Na/H exchanger (NHE3), Na/K/2Cl cotransporter (BSC1), and thiazide-sensitive Na/Cl cotransporter (TSC) proteins was determined in the kidney by Western blot analysis. Catalytic activity of Na,K-ATPase was also determined. The treatment with L-NAME significantly and steadily increased the systemic blood pressure. Total and fractional excretion of urinary sodium decreased significantly, while creatinine clearance remained unaltered. Neither plasma renin activity nor aldosterone concentration was significantly altered. The alpha1 subunit expression and the catalytic activity of Na, K-ATPase were increased in the kidney. The expression of NHE3, BSC1 and TSC was also increased significantly. These results suggest that endogenously-derived NO exerts a tonic inhibitory effect on the expression of sodium transporters, including Na, K-ATPase, NHE3, BSC1, and TSC, in the kidney.
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PMID:Increased expression of sodium transporters in rats chronically inhibited of nitric oxide synthesis. 1647 55

Previously, we demonstrated gender differences in Na-K-ATPase (NKA) expression and function after renal ischemia-reperfusion (I/R) injury (Sex differences in the alterations of Na(+), K(+)-ATPase following ischemia-reperfusion injury in the rat kidney. J Physiol 555: 471-480, 2004). Postischemic membrane destruction causes inhibition of NKA, whereas heat shock protein (HSP) 72 helps to preserve it. We tested the sex differences in postischemic expression of HSP72 and colocalization with NKA. The left renal pedicle of uninephrectomized female (F) and male (M) Wistar rats was clamped for 55 min followed by 2 (T2), 16 (T16), and 24 h (T24) of reperfusion. Uninephrectomized, sham-operated F and M rats served as controls. Postischemic blood urea nitrogen (BUN), serum creatinine, and renal histology were analyzed. HSP72 mRNA expression was detected by RT-PCR, protein levels by Western blot analysis. Fluorescent immunohistochemistry was performed to evaluate the localization of HSP72 and NKA alpha(1)-subunit. Postischemic BUN and creatinine were higher, and renal histology showed more rapid progression in M vs. F (P < 0.05). HSP72 mRNA expression was higher in F vs. M in control and in all I/R groups (P < 0.05). Similar changes were observed in HSP72 protein levels (F vs. M, P < 0.05, control, T2, T16, T24, respectively). Immunohistochemical localization of HSP72 and NKA alpha(1) was similar in control F and M. In postischemic F kidneys, the majority of NKA alpha(1) and HSP72 was colocalized on the basolateral membrane of tubular cells, whereas in M prominent staining was observed in the cytosol and apical domain. This study indicates that in female kidneys the higher basal and postischemic levels of HSP72 and different colocalization with NKA might contribute to the gender differences in renal I/R injury.
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PMID:Sex differences in heat shock protein 72 expression and localization in rats following renal ischemia-reperfusion injury. 1660 51

The present study was designed to investigate the possible potential protective role of coenzymeQ10 (CoQ10; 10 mg/kg/day, ip) and/or green tea (GT; 25mg/kg/day, po) against gentamicin (GM) nephrotoxicity. Marked increase in the level of serum urea. creatinine and lipid peroxidation (LPO) content was found after administration of gentamicin (80 mg/kg/day, ip) for eight days along with significant decrease in the antioxidant enzymes, superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT) as well as brush border enzymes (Na+/K+ ATPase, Mg(+2)ATPase and Ca2+ ATPase). Treatment with CoQ10 or green tea alone with GM showed significant decrease in serum urea, creatinine and tissue LPO content and significant increase in antioxidant and membrane bound enzymes. Combined treatment with CoQ10 and green tea was more effective in mitigating adverse effect of GM nephrotoxicity. The present work indicated that CoQ10 and green tea due to their antioxidant activity modified the biochemical changes occurred during gentamicin nephrotoxicity and thus had a potential protective effect.
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PMID:Modification of biochemical parameters of gentamicin nephrotoxicity by coenzyme Q10 and green tea in rats. 1670 97

Acute effects of mercuric chloride (HgCl2) were evaluated on mice. Mice received a single dose of HgCl2 (4.6 mg/kg, subcutaneously) for three consecutive days. Thirty minutes after the last injection with HgCl2, mice received one single injection of 2,3-dimercapto-1-propanesulfonic acid (DMPS) or N-acetylcysteine (NAC) or diphenyl diselenide (PhSe)2. DMPS, NAC and (PhSe)2 were utilized as therapy against mercury exposure. At 24 h after the last HgCl2 injection, blood, liver and kidney samples were collected. delta-Aminolevulinate dehydratase (delta-ALA-D) and Na+, K- (+) ATPase activities, thiobarbituric acid-reactive substances (TBARS), non-protein thiols (NPSH) and ascorbic acid concentrations were evaluated. Plasma aspartate (AST) and alanine (ALT) aminotransferase activities, as well as urea and creatinine levels were determined. The group of mice exposed to Hg + (PhSe)2 presented 100% of lethality. Exposure with HgCl2 caused a decrease on the body weight gain and treatments did not modify this parameter. delta-ALA-D, AST and ALT activities, TBARS, ascorbic acid levels and NPSH (hepatic and erythrocytic) levels were not changed after HgCl2 exposure. HgCl2 caused an increase in renal NPSH content and therapies did not modify these levels. Mice treated with (PhSe)2, Hg + NAC and Hg + DMPS presented a reduction in plasma NPSH levels. Creatinine and urea levels were increased in mice exposed to Hg + NAC, while Hg + DMPS group presented an increase only in urea level. Na+, K- (+) ATPase activity was inhibited in mice exposed to Hg + DMPS and Hg + NAC. In conclusion, therapies with (PhSe)2, DMPS and NAC following mercury exposure must be better studied because the formation of more toxic complexes with mercury, which can mainly damage renal tissue.
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PMID:DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury. 1684 Dec 48

Extracellular calcium concentrations in humans are thousands times higher than within cells. Maintenance of such gradient requires specific regulation including intracellular stores, Ca binding proteins and transmembrane protein systems. The aim of the study was to estimate PMCA (plasma membrane Ca-transporting adenosine triphosphatase; ATPase 3.6.1.38) activity and calcium homeostasis in erythrocytes of children with chronic kidney disease (CKD). Twenty-one children wth CKD stages 1-3 (group I) and 18 healthy children (group II) were examined. Group I was divided into two subgroups: Ia (8 patients with normal intact parathyroid hormone, iPTH, serum levels) and Ib (13 patients with increased iPTH). iPTH, urea, creatinine, inorganic phosphorus, cytosolic Ca2+ in red blood cells (R-Ca), and PMCA were determined. Significantly elevated R-Ca levels were observed in children from subgroup Ib in comparison with group II and subgroup Ia. The lowest activity of PMCA was found in subgroup Ia and Ib in comparison with group II. There was a negative correlation between PMCA and R-Ca in group Ia and Ib (r=-0.8, r=-0.9, respectively). In children with CKD treated conservatively, activity of PMCA in erythrocytes is disturbed. An increase in R-Ca and decrease in PMCA activity are also observed.
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PMID:Ca2+-Mg2+-dependent ATP-ase activity and calcium homeostasis in children with chronic kidney disease. 1710 39

Pepticare, a herbomineral formulation, was administered orally to rats at the dose levels of 125, 250, 500 and 1000 mg/kg to investigate its effect on isoproterenol-induced myocardial infarction and cisplatin-induced renal damage. The drug reduced the levels of serum creatine kinase (CK), glutamic oxaloacetate transaminase (GOT), lactate dehydrogenase (LDH) and uric acid in isoproterenol-induced cardiac damage. In cisplatin-induced renal damage, Pepticare reduced the serum levels of creatinine, urea, blood urea nitrogen (BUN) and uric acid. It was further found that administration of Pepticare increased the levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), membrane bound enzymes like Ca2+ ATPase, Mg2+ ATPase and Na+ K+ ATPase and decreased lipid peroxidation (MDA) in heart and kidney, respectively. Thus it can be concluded that Pepticare possesses antioxidant activity and protects the heart and kidney from damage caused by isoproterenol and cisplatin, respectively.
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PMID:Antioxidant activity of Pepticare, a herbomineral formulation, in experimentally induced renal and cardiac damage. 1713 56


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