title: Reduced arteriolar responses to skeletal muscle contraction after ingestion of a high salt diet.
abstract: 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(G)-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.
authors.affiliation: Department of Physiology and Pharmacology, and Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, Morgantown, WV 265056-9229, USA.
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Marvar
authors.forename: Timothy R
authors.initials: TR
authors.lastname: Nurkiewicz
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Boegehold
mesh_terms: D000818:Animals; D001160:Arterioles / Q000502:physiology*; D001682:Biological Availability; D001810:Blood Volume; D004305:Dose-Response Relationship, Drug; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology*; D009569:Nitric Oxide / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000494:pharmacology
chemical_list: D017382:Reactive Oxygen Species; D017673:Sodium Chloride, Dietary; D009569:Nitric Oxide