title: Nitric oxide in afferent arterioles after uninephrectomy depends on extracellular L-arginine.
abstract: Uninephrectomy (UNX) causes hyperperfusion of the contralateral remaining kidney via increased nitric oxide (NO) synthesis. Although the exact mechanism remains largely unknown, we hypothesize that this would be localized to the afferent arteriole and that it depends on cellular uptake of l-arginine. The experiments were performed in rats 2 days (early) or 6 wk (late) after UNX and compared with controls (Sham) to study acute and chronic effects on NO metabolism. Renal blood flow was increased after UNX (21 ± 2 ml·min(-1)·kg(-1) in sham, 30 ± 3 in early, and 26 ± 1 in late, P < 0.05). NO inhibition with N(ω)-nitro-L-arginine methyl ester hydrochloride (L-NAME) caused a greater increase in renal vascular resistance in early UNX compared with Sham and late UNX (138 ± 24 vs. 88 ± 10, and 84 ± 7%, P < 0.01). The lower limit of autoregulation was increased both in early and late UNX compared with Sham (P < 0.05). L-NAME did not affect the ANG II-induced contraction of isolated afferent arterioles (AA) from Sham. AA from early UNX displayed a more pronounced contraction in response to L-NAME (-57 ± 7 vs. -16 ± 7%, P < 0.05) and in the absence of L-arginine (-41 ± 4%, P < 0.05) compared with both late UNX and Sham. mRNA expression of endothelial NO synthase was reduced, whereas protein expression was unchanged. Cationic amino acid transporter-1 and -2 mRNA was increased, while protein was unaffected in isolated preglomerular resistance vessels. In conclusion, NO-dependent hyperperfusion of the remaining kidney in early UNX is associated with increased NO release from the afferent arteriole, which is highly dependent on extracellular L-arginine availability.
authors: Renal Research Group, Institute of Medicine, University of Bergen, Bergen, Norway.
authors: Frank
authors: F
authors: Helle
authors: Trude
authors: T
authors: Skogstrand
authors: Idit F
authors: IF
authors: Schwartz
authors: Doron
authors: D
authors: Schwartz
authors: Bjarne M
authors: BM
authors: Iversen
authors: Fredrik
authors: F
authors: Palm
authors: Michael
authors: M
authors: Hultström
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000378:metabolism*; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D005919:Glomerular Filtration Rate / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009392:Nephrectomy; D009569:Nitric Oxide / Q000378:metabolism*; D009929:Organ Size / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester