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

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, [10.sup.-4] M) increased proximal fluid uptake ([J.sub.va], at 2.47 [+ or -] 0.61 x [10.sup.-4] [mm.sup.3] [multiplied by] [mm.sup.-2] [multiplied by] [s.sup.-1]) by 17% (P [is less than] 0.05), whereas coadministration with sodium nitroprusside (SNP, [10.sup.-4] M) decreased [J.sub.va] by 18% (P [is less than] 0.01). Similar manipulation of NO generation was without effect in groups of Wistar rats subjected to acute renal denervation. Intratubular aminoguanidine ([10.sup.-4] M), a selective inducible nitric oxide synthase (NOS) blocker, had no effect on [J.sub.va] in intact kidneys of Wistar rats, but the neuronal NOS (nNOS) blocker, 7-nitroindazole ([10.sub.-4] M and [10.sup.-6] M) increased [J.sub.va] by 19-23% (both P [is less than] 0.001). In stroke-prone spontaneously hypertensive rats (SHRSP), [J.sub.va] values in the innervated kidneys were lower (P [is less than] 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