Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
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.
 ...
PMID:Features of gentamicin nephrotoxicity and effect of concurrent cephalothin in the rat. 687 60