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Am J Physiol Renal Physiol (January 29, 2002). doi:10.1152/ajprenal.00330.2001
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Articles in PresS, published online ahead of print January 28, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00330.2001
Submitted on October 30, 2001
Accepted on January 24, 2002

Glucose Stimulates O2 Consumption, NOS and Na/H Exchange in Diabetic Rat Proximal Tubules

Andrew D Baines1 and Patrick Ho1*

1 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada

eNOS and nNOS protein increased in proximal tubules of acidotic diabetic rats 3-5 weeks after streptozotocin injection. NOS activity (citrulline production) was similar in non-diabetic and diabetic tubules incubated with low glucose (5 mM + 20 mM mannitol); but after 30 minutes with high glucose (25 mM), Ca-sensitive citrulline production had increased 23% in diabetic tubules. Glucose concentration did not influence citrulline production in non-diabetic tubules. High glucose increased cpt10-scavenged NO sevenfold in a suspension of diabetic tubules but did not alter NO in non-diabetic tubules. Diabetes increased ouabain-sensitive 86Rb-uptake (141±9 vs 122±6 nmol/min.mg) and oligomycin-sensitive O2 consumption (QO2) (16.0±1.7 vs 11.3±0.7 nmol/min.mg). EIPA-inhibitable QO2 (6.5±0.6 vs 2.4±0.3 nmol/min.mg) accounted for increased oligomycin-sensitive QO2 in diabetic tubules. L-NAME inhibited most of the increase in Rb-uptake and QO2 in diabetic tubules. L-NAME had little effect in non-diabetic tubules. Inhibition of QO2 by EIPA and L-NAME was only 5-8% additive. Conclusion: uncontrolled diabetes for 3-5 weeks increases NOS protein in proximal tubules and makes NOS activity sensitive to glucose concentration. Under these conditions NO stimulates NaKATPase and QO2in proximal tubules.




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