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      Lack of a Role of Neuronal Nitric Oxide Synthase in the Regulation of the Renal Function in Rats Fed a Low-Sodium Diet

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          Background/Aims: It has been shown that nitric oxide (NO) generated from neuronal NO synthase (nNOS) counteracts angiotensin II mediated vasoconstriction in the pre- and in the postglomerular microcirculation. Previous studies have demonstrated that the nNOS expression in the macula densa of the renal cortex is enhanced by dietary salt restriction. In view of the well-known fact that dietary salt restriction also leads to an activation of the renin-angiotensin system, the present study was performed to assess the role of nNOS-derived NO in the regulation of the renal function in rats maintained on control (C) and low-salt (LS) diets. Methods: Groups of rats were fed either the C or the LS diet. On day 13 after adaptation to the appropriate diet, renal clearance studies were performed to determine the effects of acute nNOS inhibition either by S-methyl- L-thiocitrulline ( L-SMTC) or by N<sup>ω</sup>-propyl- L-arginine ( L-NPA) on renal hemodynamics and sodium excretory function. In separate groups of rats maintained on either the C or the LS diet, the mRNA levels of nNOS and of renin in the renal cortex were examined using the semiquantitative reverse-transcriptase polymerase chain reaction. Results: Intrarenal infusion of vehicle (0.9% saline; 4 µl/min) did not change glomerular filtration rate (GFR), renal plasma flow (RPF), or sodium excretion in either C diet or LS diet rats. Acute intrarenal infusion of L-SMTC (0.3 mg/h) and L-NPA (0.01 mg/h) decreased GFR (–14 ± 5 vs. –13 ± 3%), RPF (–19 ± 6 vs. –17 ± 5%), and sodium excretion (–17 ± 5 vs. –16 ± 4%) in C diet rats as compared with control values (p < 0.05). In contrast, in LS rats, intrarenal administration of either L-SMTC or L-NPA did not cause significant changes in GFR, RPF, and sodium excretion. Furthermore, the mRNA expression for nNOS in the renal cortex was moderately increased in LS rats as compared with C rats (densitometric ratios of nNOS mRNA/GAPDH mRNA 0.31 ± 0.01 vs. 0.22 ± 0.04, p < 0.05), in parallel with the renin expression (renin mRNA/GAPDH mRNA ratios 1.4 ± 0.2 vs. 1.0 ± 0.1, p < 0.05). Conclusions: These results indicate that in normotensive rats kept on a normal salt intake nNOS-derived NO modulates both afferent and efferent arteriolar tones. In contrast, rats on an LS diet exhibit an impaired renal vascular responsiveness to nNOS-derived NO or an impaired ability to release NO by nNOS despite enhanced expression of nNOS mRNA in the renal cortex. In addition, the lack of effect of acute nNOS inhibition on renal function suggests that NO derived by nNOS does not participate in counteracting the vasoconstrictor influences of elevated circulating and/or intrarenal angiotensin II levels on pre- and postglomerular microcirculation in rats on an LS diet.

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          Oxidative stress and vascular damage in hypertension.

          Oxidative stress, a state of excessive reactive oxidative species activity, is associated with vascular disease states such as hypertension. In this review, we discuss the recent advances in the field of reactive oxidative species-mediated vascular damage in hypertension. These include the identification of redox-sensitive tyrosine kinases, the characterization of enzymatic sources of superoxide production in human blood vessels, and their relationship with vascular damage in atherosclerosis and hypertension. Finally, recent developments in the search for strategies to attenuate vascular oxidative stress are reviewed.
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                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                08 November 2002
                : 25
                : 4
                : 224-231
                aDepartment of Experimental Medicine, Institute for Clinical and Experimental Medicine, Center for Experimental Cardiovascular Research, Prague, Czech Republic; bSection of Nephrology, Department of Medicine, Medical Policlinic, University of Bonn, Germany
                66350 Kidney Blood Press Res 2002;25:224–231
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, References: 35, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/66350
                Original Paper


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