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)

Since the mechanisms responsible for stimulation of kidney Na-K-ATPase during streptozotocin-induced diabetes are unknown, we studied the possible role(s) of kidney hyperfiltration and hypertrophy and of hyperaldosteronism on Na-K-ATPase induction. For this purpose, we studied the relationship between Na-K-ATPase activity in individual nephron segments and alterations of glomerular filtration rate during the early phase of diabetes. Within 2 days after streptozotocin administration, Na-K-ATPase activity markedly increased in the proximal convoluted tubule, medullary thick ascending limb and cortical and outer medullary collecting tubule, but not in the proximal straight tubule, cortical thick ascending limb and distal convoluted tubule. Streptozotocin administration also markedly enhanced the glomerular filtration rate but only after 4 days following initiation of treatment. Changes in Na-K-ATPase were specific since the activity of adenylate cyclase, another marker of basolateral membranes, was not altered. Finally, when animals were adrenalectomized prior to streptozotocin treatment, Na-K-ATPase stimulation was curtailed in the collecting tubule but not in more proximal segments. These results suggest that diabetes alters Na-K-ATPase activity in specific nephron segments independent of alterations of glomerular filtration rate and of kidney hypertrophy, and that the stimulation of collecting tubule Na-K-ATPase is secondary to hyperaldosteronism.
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PMID:Mechanism of increased tubular Na-K-ATPase during streptozotocin-induced diabetes. 281 17

Renal hypertrophy is a common consequence of diabetes mellitus that precedes and possibly accounts for the increased glomerular filtration rate. We have postulated that the glucose-mediated increase in the intracellular concentration of sodium [Na]i initiates the chain of events leading to the increase in cell size and eventually cell number. Experiments were conducted on Sprague-Dawley rats made diabetic by the intravenous injection of 45 mg/kg body wt of streptozotocin dissolved in a 5 mM citrate buffer solution. Control animals were injected with the vehicle alone. Ninety-six hours and 11 weeks later, measurements of [Na]i were done by NMR spectroscopy on suspensions of proximal tubules, using dysprosium tripolyphosphate as an extracellular shift reagent. At 96 hours after the induction of the diabetes, there was a 60% increase in [Na]i compared to control (P less than 0.01). No further increase in [Na]i was observed during the subsequent 11 weeks of observation. Addition of ouabain (1.0 mM) resulted in a fourfold increase in [Na]i in tubules from control animals, and a 2.5-fold increase in tubules from 96-hour diabetic rats. Ouabain-inhibitable Na+-K+-ATPase activity was substantially higher in the renal tubules of diabetic rats, the increase being proportional to that of [Na]i. In order to ascertain the effect of hyperglycemia on [Na]i, proximal tubules prepared from kidneys of normal and diabetic rats were exposed to low (5 mM) and high (25 mM) concentration of glucose in the media.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular sodium in proximal tubules of diabetic rats. Role of glucose. 338 34