AFLUID October 46/4

Wu, Xiao Chun, Peter J. Harris, and Edward J. Johns. Nitric oxide and renal nerve-mediated proximal tubular reabsorption in normotensive and hypertensive rats. Am. J. Physiol. 277 (Renal Physiol. 46): F560–F566, 1999.—In Inactin-anesthetized Wistar rats with an intact renal innervation, intratubular nitro-L-arginine methyl ester (L-NAME, 1024 M) increased proximal fluid uptake (Jva, at 2.47 6 0.61 3 1024 mm3·mm22 ·s21) by 17% (P , 0.05), whereas coadministration with sodium nitroprusside (SNP, 1024 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 (1024 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 (1024 M and 1026 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.