Nitric oxide and renal nerve-mediated proximal tubular reabsorption in normotensive and hypertensive rats
Wu, X.C.; Harris, P.J.; Johns, E.J.
American Journal of Physiology 277(4): F560-F566
1999
ISSN/ISBN: 0002-9513 PMID: 10516280 Document Number: 509693
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 mm-3.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 (104 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. Reprinted by permission of the publisher.