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Am J Physiol Renal Physiol 277: F560-F566, 1999;
0363-6127/99 $5.00
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Vol. 277, Issue 4, F560-F566, October 1999

Nitric oxide and renal nerve-mediated proximal tubular reabsorption in normotensive and hypertensive rats

Xiao Chun Wu1, Peter J. Harris2, and Edward J. Johns1

1 Department of Physiology, Medical School, University of Birmingham, Birmingham B15 2TT, United Kingdom; and 2 Department of Physiology, University of Melbourne, Parkville, Victoria 3052, Australia

In Inactin-anesthetized Wistar rats with an intact renal innervation, intratubular nitro-L-arginine methyl ester (L-NAME, 10-4 M) increased proximal fluid uptake (Jva, at 2.47 ± 0.61 × 10-4 mm3 · mm-2 · s-1) by 17% (P < 0.05), whereas coadministration with sodium nitroprusside (SNP, 10-4 M) decreased Jva by 18% (P < 0.01). Similar manipulation of NO generation was without effect in groups of Wistar rats subjected to acute renal denervation. Intratubular aminoguanidine (10-4 M), a selective inducible nitric oxide synthase (NOS) blocker, had no effect on Jva in intact kidneys of Wistar rats, but the neuronal NOS (nNOS) blocker, 7-nitroindazole (10-4 M and 10-6 M) increased Jva by 19-23% (both P < 0.001). In stroke-prone spontaneously hypertensive rats (SHRSP), Jva values in the innervated kidneys were lower (P < 0.05) than in the corresponding Wistar groups and were unchanged by intratubular L-NAME or L-NAME plus SNP. The tonic attenuation of proximal epithelial transport by NO was dependent on the renal sympathetic nerves and appeared to be generated by the nNOS isoform of the enzyme. This role of NO was not evident in the SHRSP.

nitric oxide synthase; renal sympathetic nerves; proximal tubular sodium reabsorption; stroke-prone spontaneously hypertensive rats


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