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      Reduced Arteriolar Responses to Skeletal Muscle Contraction after Ingestion of a High Salt Diet

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          We previously reported that in skeletal muscle arterioles of rats fed a very high salt (HS; 7%) diet, the bioavailability of endothelium-derived nitric oxide (NO) is reduced through scavenging by reactive oxygen species. Because arteriolar NO can play an important role in local blood flow control, we investigated whether arteriolar responses to increased tissue metabolism become compromised in skeletal muscle of salt-fed rats. Consumption of a HS (4%) diet for 4 weeks had no effect on arteriolar diameters, volume flow or shear stress in resting spinotrapezius muscle. Arteriolar responses to a modest elevation in metabolic demand (0.5 Hz contraction) were not different from those in rats fed a normal diet, but diameter responses to a greater elevation in metabolic demand (4 Hz contraction) were significantly less in HS rats than in rats fed a normal diet. In both groups, the NO synthase inhibitor N<sup>G</sup>-monomethyl- L-arginine reduced resting arteriolar diameters and flow by a similar amount and had little or no effect on arteriolar diameter or flow responses to muscle contraction. Arterioles in HS rats exhibited an increase in overall oxidant activity (tetranitroblue tetrazolium reduction) but not in superoxide activity (dihydroethidine oxidation). Reactive oxygen species scavengers (2,2,6,6-tetramethylpiperidine-N-oxyl and catalase) did not normalize the reduced arteriolar responses to muscle contraction in HS rats. These findings suggest that increased oxidant activity in the arteriolar network of salt-fed rats is not due to accumulation of superoxide anion and that neither this oxidant activity nor reduced NO availability can account for the blunted active arteriolar dilation in rats fed a 4% salt diet.

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          Most cited references 11

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          Skeletal muscle arteriolar reactivity in SS.BN13 consomic rats and Dahl salt-sensitive rats.

          Previous studies have demonstrated that angiotensin II is a crucial factor in maintaining normal vascular reactivity. In this study, we tested the hypothesis that altered reactivity to vasoactive stimuli in Dahl salt-sensitive (S) rats on a high salt diet could be prevented by introgression of chromosome 13 from the normotensive Brown Norway strain, which carries a normally functioning renin gene. Dahl S and consomic SS.BN13 rats were fed a low salt (0.4%) or high salt diet (4%) for 4 to 6 days or 4 weeks. Arteriolar responses to elevated superfusion solution PO2, acetylcholine, and sodium nitroprusside were assessed by videomicroscopy in the cremaster muscle. Arteriolar dilation to sodium nitroprusside was normal in both strains. Arteriolar constriction to elevated PO2 was enhanced in Dahl S and SS.BN13 rats on a high salt diet compared with responses in rats on a low salt diet. Arterioles of Dahl S rats on a high salt diet had an impaired dilation to acetylcholine, whereas dilator responses to acetylcholine were restored in SS.BN13 rats regardless of elevated salt intake. These data suggest that (1) restitution of normal renin control mechanisms by chromosomal transfer contributes to the recovery of dilator responses in SS.BN13 rats versus Dahl S rats but does not affect constrictor responses to oxygen, and (2) factors in the Dahl S genetic background contribute to an enhanced sensitivity of arterioles to elevated PO2 independent of elevated blood pressure.
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            Critical evaluation of the use of hydroethidine as a measure of superoxide anion radical

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              Reactive oxygen species and vascular signal transduction mechanisms.

              Sources of reactive O2 species in the vessel wall that potentially contribute to the control of vascular tone include NADPH oxidases, arachidonic acid metabolizing enzymes, xanthine oxidase, nitric oxide synthase and mitochondria. Specific physiological stimuli (such as changes in PO2) as well as pathophysiological stimuli control the production of reactive O2 species by many of these sources. Certain key reactive O2 species activate specific signalling mechanisms that control vascular tone, often through processes involving the metabolism of these species. The production of prostaglandins and cyclic GMP are some of the most sensitive systems regulated by hydrogen peroxide; whereas the conversion of nitric oxide (NO) to peroxynitrite (ONOO-) and inhibition of the stimulation of the cytosolic form of guanylate cyclase are processes that are very sensitive to superoxide anion (O2.-). High levels of NO production readily result in the formation of significant amounts of ONOO-, because NO competes with superoxide dismutase for the metabolism of cellular O2.- and thereby activates additional signalling mechanisms such as regulation through thiol nitrosation. As the levels of individual reactive O2 species increase, other signalling mechanisms likely to participate in vascular responses to oxidant injury seem to become activated. Thus, evidence is developing to support the concept that reactive O2 species are important contributors to the control of vascular tone.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                June 2005
                03 June 2005
                : 42
                : 3
                : 226-236
                Department of Physiology and Pharmacology, and Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, Morgantown, W. Va., USA
                85461 J Vasc Res 2005;42:226–236
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 2, References: 49, Pages: 11
                Research Paper


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