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)

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.
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PMID:Effect of potassium depletion on ischemic renal failure. 253 74

Changes in renal function, Na+-K+-ATPase activity and PAH transport system in kidney cortex were studied in rats treated with cadmium. Subcutaneous injections of CdCl2 (2 mg Cd/kg.day) for 16 days induced a marked polyuria and a hyposthenuria. These changes were accompanied by increase in urinary protein, glucose, urea, calcium, phosphate, chloride and potassium excretions. The change in urine flow was proportional to the change in total osmotic solute excretion. Creatinine excretion and TcH2O remained unchanged. Na+ excretion was not increased, but the Na+-K+-ATPase of renal cortex was significantly inhibited. PAH uptake by renal cortical slices was markedly attenuated in Cd-treated rats. The Vmax for active PAH influx was drastically reduced, but the Km was not changed. The passive influx and efflux of PAH across the basolateral membrane and the renal tissue oxygen consumption were not apparently altered in Cd-treated animals. These results indicate that 1) the nature of Cd-induced polyuria and hyposthenuria is an osmotic diuresis induced by proximal tubular rejection of various substances, and 2) the mechanism of impaired renal PAH excretion in Cd-treated animals is a loss of organic anion carriers in proximal tubular basolateral membranes.
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PMID:Changes in renal function in cadmium-intoxicated rats. 285 38

Reversal of myocardial biochemical changes with insulin treatment (4 and 8 wk) was studied in 8 and 12 wk streptozotocin (STZ)-diabetic rats. STZ-induced diabetes was characterized by elevations in blood glucose, serum cholesterol, and triglycerides and depressed serum insulin levels. Insulin treatment for 4 and 8 wk completely restored the serum alterations to control values. The polyuria, polydipsia, and polyphagia were also markedly diminished by the insulin treatment. Diabetic rats had pronounced decreases in body, heart, and left ventricular weights, all of which were completely reversed by the insulin treatment. Hydroxyproline accumulation in diabetic rat hearts was only reversed by the 8-wk and not by the 4-wk insulin treatment. STZ produced a significant depletion of left ventricular magnesium content as well as depression of K+-stimulated sarcoplasmic reticulum and myofibrillar ATPase activities. Both the 4- and 8-wk insulin treatment produced a complete recovery of the myocardial magnesium content. No significant changes in sarcolemmal Na+-K+-ATPase and K+-stimulated p-nitrophenyl phosphatase activities were observed in diabetic animals compared with control. The decreased latency of the lysosomal hydrolase, N-acetyl-beta-glucosaminidase, and the increased collagen deposition observed in the diabetic hearts were only partially reversed by the 4-wk insulin treatment, but completely reversed by the 8-wk treatment period.
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PMID:Insulin reversal of biochemical changes in hearts from diabetic rats. 294 95

Single administration per os of the 0.066 M LiCl solution (3 ml per 100 g body weight) caused natriuresis. In the "lithium" rats with prolonged lithium treatment (i.p. injections during 10 days), polyuria developed; after water or 0.9% NaCl load excretion of Na, K, Ca, Mg and water increased as compared to the control rats. The saluretic effect was very obvious after 0.9% NaCl load in the "lithium" rats. The Na, K ATPase activity was measured by the quantitative cytochemical method, decreased only in the collecting ducts of the "lithium" rats. The natriuretic effect of acute lithium administration seems to be due to a lowering of the sodium proximal reabsorption. Prolonged lithium treatment suppresses the sodium transport in the collecting ducts.
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PMID:[Effect of lithium on the renal excretory function and Na, K-ATPase activity in rats]. 627 3

Acute renal failure was induced in rats by injection of a lethal dose of live Escherichia coli. Enzyme activities of the proximal tubule were studied histochemically at three, six, and 12 hours following E coli injection. The enzymes examined were alkaline phosphatase (A1Pase), acid phosphatase (AcPase), adenosine triphosphatase (ATPase), succinate dehydrogenase (SDH), glucose-6-phosphatase (G6Pase), and glucose-6-phosphate dehydrogenase (G6PDH). At three hours, ATPase activity was slightly decreased, while other enzymes showed no changes in activities at this time. At six hours, a slight increase in AcPase activity was seen in the pars recta. At this time, although A1Pase showed no change in activity, other enzymes revealed slight decreases in activities: G6Pase and SDH in the pars convoluta, ATPase in the pars convoluta and pars recta, and G6PDH in pars recta. At 12 hours after treatment, all enzymes showed decreases in activities; however, no necrotic tubule changes were detectable by light microscopy. Since sodium reabsorption in proximal tubules requires a sodium pump consisting of Na-K ATPase, early histochemical changes in ATPase activity in proximal tubule following bacteremia may be related to early changes in sodium reabsorption causing polyuria and to the subsequent development of acute renal failure.
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PMID:The pathophysiology of septic shock: acute renal failure in rats following live E coli injection. A histochemical study of the proximal tubules. 629 45

Sprague-Dawley rats given gentamicin from 10 to 70 mg/kg/day for 9 days showed a linear decrease in glomerular filtration rate with increasing dose, paralleled by histologic changes of acute tubular necrosis and cast formation only at the higher doses. Nephrotoxicity was correlated with the peak, rather than trough, serum gentamicin levels in this study, suggesting that it is the mean level of gentamicin over time that determines renal injury. The polyuria caused by gentamicin resulted mainly from a tubular concentrating defect rather than enhanced sodium or osmolal excretion and may be explained by the finding of a predominance of casts in the medullary thin limbs of the loops of Henle. No effect of gentamicin on the activity of cortical or medullary sodium-potassium adenosine triphosphatase was found to account for the modest sodium wasting. Concurrent administration of sodium cephalothin decreased the renal toxicity of gentamicin at high doses, an effect not explained by the added sodium or nonreabsorbable anion.
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PMID:Features of gentamicin nephrotoxicity and effect of concurrent cephalothin in the rat. 687 60

Lithium (Li) treatment is often associated with nephrogenic diabetes insipidus (NDI). The changes in whole kidney expression of aquaporin-1 (AQP1), -2, and -3 as well as Na-K-ATPase, type 3 Na/H exchanger (NHE3), type 2 Na-Pi cotransporter (NaPi-2), type 1 bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1), and thiazide-sensitive Na-Cl cotransporter (TSC) were examined in rats treated with Li orally for 4 wk: protocol 1, high doses of Li (high Na(+) intake), and protocol 2, low doses of Li (identical food and normal Na(+) intake in Li-treated and control rats). Both protocols resulted in severe polyuria. Semiquantitative immunoblotting revealed that whole kidney abundance of AQP2 was dramatically reduced to 6% (protocol 1) and 27% (protocol 2) of control levels. In contrast, the abundance of AQP1 was not decreased. Immunoelectron microscopy confirmed the dramatic downregulation of AQP2 and AQP3, whereas AQP4 labeling was not reduced. Li-treated rats had a marked increase in urinary Na(+) excretion in both protocols. However, the expression of several major Na(+) transporters in the proximal tubule, loop of Henle, and distal convoluted tubule was unchanged in protocol 2, whereas in protocol 1 significantly increased NHE3 and BSC-1 expression or reduced NaPi-2 expression was associated with chronic Li treatment. In conclusion, severe downregulation of AQP2 and AQP3 appears to be important for the development of Li-induced polyuria. In contrast, the increased or unchanged expression of NHE3, BSC-1, Na-K-ATPase, and TSC indicates that these Na(+) transporters do not participate in the development of Li-induced polyuria.
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PMID:Altered expression of renal AQPs and Na(+) transporters in rats with lithium-induced NDI. 1096 35

Diabetes mellitus (DM) is associated with osmotic diuresis and natriuresis. At day 15, rats with DM induced by streptozotocin (n = 13) had severe hyperglycemia (27.1 +/- 0.4 vs. 4.7 +/- 0.1 mM in controls) and had a fivefold increase in water intake (123 +/- 5 vs. 25 +/- 2 ml/day) and urine output. Semiquantitative immunoblotting revealed a significant increase in inner medullary AQP2 (201 +/- 12% of control rats, P < 0.05) and phosphorylated (Ser(256)) AQP2 (p-AQP2) abundance (299 +/- 32%) in DM rats. Also, the abundance of inner medullary AQP3 was markedly increased to 171 +/- 19% of control levels (100 +/- 4%, n = 7, P < 0.05). In contrast, the abundance of whole kidney AQP1 (90 +/- 3%) and inner medullary AQP4 (121 +/- 16%) was unchanged in rats with DM. Immunoelectron microscopy further revealed an increased labeling of AQP2 in the apical plasma membrane of collecting duct principal cells (with less labeling in the intracellular vesicles) of DM rats, indicating enhanced trafficking of AQP2 to the apical plasma membrane. There was a marked increase in urinary sodium excretion in DM. Only Na(+)/H(+) exchanger NHE3 was downregulated (67 +/- 10 vs. 100 +/- 11%) whereas there were no significant changes in abundance of type 2 Na-phosphate cotransporter (128 +/- 6 vs. 100 +/- 10%); the Na-K-2Cl cotransporter (125 +/- 19 vs. 100 +/- 10%); the thiazide-sensitive Na-Cl cotransporter (121 +/- 9 vs. 100 +/- 10%); the alpha(1)-subunit of the Na-K-ATPase (106 +/- 7 vs. 100 +/- 5%); and the proximal tubule Na-HCO(3) cotransporter (98 +/- 16 vs. 100 +/- 7%). In conclusion, DM rats had an increased AQP2, p-AQP2, and AQP3 abundance as well as high AQP2 labeling of the apical plasma membrane, which is likely to represent a vasopressin-mediated compensatory increase in response to the severe polyuria. In contrast, there were no major changes in the abundance of AQP1, AQP4, and several major proximal and distal tubule Na(+) transporters except NHE3 downregulation, which may participate in the increased sodium excretion.
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PMID:Compensatory increase in AQP2, p-AQP2, and AQP3 expression in rats with diabetes mellitus. 1124 63

The aim of this study was to detect a relationship between hemodynamic disorders in patients with hemorrhagic fever with the renal syndrome (HFRS) and erythrocyte aggregability and erythrocyte membrane ATPase activity. A total of 100 patients with HFRS of different severity were examined. Central hemodynamic parameters were studied: circulating blood volume, minute volume, cardiac index, stroke volume, and total peripheral vascular resistance during preoliguria, oliguria, and polyuria periods. Blood parameters were studied: percentage of minimum and maximum aggregation, disaggregation coefficient, activities of transport adenosine triphosphatases (Na, K, and Ca-activated ATPases and Mg-dependent ATPase). The main hemodynamic parameters were increased (p < 0.05) during early preoliguria and decreased during oliguria; during the polyuria period they again corresponded to the hyperkinetic circulation. The minimum erythrocyte aggregation increased by 110 and 130% in medium-severe and severe HFRS, respectively, the maximum erythrocyte aggregation by 20 and 28%, respectively (p < 0.05). Disaggregation coefficient decreased by 55%. The activities of Na, K(+)-ATPases decreased by 13% during preoliguria period, by 17.5% during oliguria, and by 11.7% during polyuria (p < 0.05) in patients with moderate disease. In severe disease these decreases were 14, 19, and 15%, respectively (p < 0.05). Similar changes were observed in the activities of Ca(++)-ATPase and Mg-dependent ATPase. Hence, the detected hemodynamic changes in patients with medium-severe and severe HFRS correlated with disorders in erythrocyte aggregability and decreased activity of transport ATPases, which can be used for evaluation of the severity of clinical condition and early diagnosis.
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PMID:[Central hemodynamic disorders and rheological red blood cell properties in hemorrhagic fever patients with renal syndrome]. 1151 Jan 83

Chronic hypercalcemia (HC) is accompanied by urinary concentration defects, and functional studies indicate defects in the thick ascending limb (TAL). We hypothesize that dysregulation of renal sodium transporters may play an important role in this. Vitamin D-induced HC in rats resulted in polyuria, natriuresis, and phosphaturia. Immunoblotting revealed a marked reduction in the abundance of rat type 1 bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1) in inner stripe of the outer medullary (ISOM; 36 +/- 5%) and whole kidney (51 +/- 11%) in HC. Consistent with this finding, immunocytochemistry and immunoelectron microscopy demonstrated reduced BSC-1 labeling of the apical plasma membrane. Immunoblotting and immunohistochemical labeling of the K channel Kir 1.1 (ROMK) was also reduced in HC. In contrast, there were no reductions in the expression of Na/H exchanger (NHE)3 and Na,K-ATPase in ISOM. The abundance of the proximal tubule type II Na-P(i) cotransporter (NaPi-2) (but not Na,K-ATPase and NHE3) was significantly reduced (25 +/- 4%), consistent with a dramatic increase in urinary phosphate excretion. In conclusion, 1) the reduced abundance of BSC-1 and ROMK in TAL is likely to play a major role in the urinary concentration defects associated with HC and 2) the reduced abundance of NaPi-2 is likely to play a role in the increased urinary phosphate excretion.
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PMID:Reduced expression of Na-K-2Cl cotransporter in medullary TAL in vitamin D-induced hypercalcemia in rats. 1173 10


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