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1 Division of Nephrology-Hypertension, University of California, San Diego, San Diego, California, United States; Stein Institute for Research on Aging, University of California, San Diego, San Diego, California, United States
2 Division of Nephrology-Hypertension, University of California, San Diego, San Diego, California, United States
3 Division of Nephrology-Hypertension, University of California, San Diego, United States
4 Department of Medicine and Cancer Center, University of California, San Diego, San Diego, California, United States
* To whom correspondence should be addressed. E-mail: rblantz{at}ucsd.edu.
The tubuloglomerular feedback (TGF) system serves to establish an appropriate balance between tubular reabsorption and glomerular filtration rate (GFR). High salt at the macula densa activates TGF to decrease GFR. Effector molecules for the TGF signal include ATP and adenosine. Over time the GFR will adapt by increasing even if a high salt concentration persists. A potential modulator of this TGF adaptation is NOS-1 derived nitric oxide (NO). In isolated glomerular preparations we developed a system to evaluate the effects of changing dietary salt on ecto-5'-nucleotidase (ecto-5'-NT) activity, the final enzyme in the conversion of ATP to adenosine. We find observable ecto-5'-NT activity in isolated glomeruli, and that this activity can be regulated by salt diet, with high salt increasing activity. Conversely, NO decreases ecto-5'-NT activity in glomerular preparations. Moreover, NO inhibition of ecto-5'-NT activity is suppressed in the presence of dithiothreitol, suggesting nitrosylation as a reversible, oxidative-stress sensitive mechanism. The salt induced activation of ecto-5'-NT would be in accord with salt activation of TGF. NO inhibition of the enzyme could be part of the adaptive phase.
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