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dc.contributor.authorFerguson, SK
dc.contributor.authorGlean, AA
dc.contributor.authorHoldsworth, CT
dc.contributor.authorWright, JL
dc.contributor.authorFees, AJ
dc.contributor.authorColburn, TD
dc.contributor.authorStabler, T
dc.contributor.authorAllen, JD
dc.contributor.authorJones, AM
dc.contributor.authorMusch, TI
dc.contributor.authorPoole, DC
dc.date.accessioned2016-03-01T15:27:37Z
dc.date.issued2016-03
dc.description.abstractThe nitric oxide synthase (NOS)-independent pathway of nitric oxide (NO) production in which nitrite (NO2 (-)) is reduced to NO may have therapeutic applications for those with cardiovascular diseases in which the NOS pathway is downregulated. We tested the hypothesis that NO2 (-) infusion would reduce mean arterial pressure (MAP) and increase skeletal muscle blood flow (BF) and vascular conductance (VC) during exercise in the face of NOS blockade via L-NAME. Following infusion of L-NAME (10 mg kg(-1), L-NAME), male Sprague-Dawley rats (3-6 months, n = 8) exercised without N(G)-nitro-L arginine methyl ester (L-NAME) and after infusion of sodium NO2 (-) (7 mg kg(-1); L-NAME + NO2 (-)). MAP and hindlimb skeletal muscle BF (radiolabeled microsphere infusions) were measured during submaximal treadmill running (20 m min(-1), 5% grade). Across group comparisons were made with a published control data set (n = 11). Relative to L-NAME, NO2 (-) infusion significantly reduced MAP (P < 0.03). The lower MAP in L-NAME+NO2 (-) was not different from healthy control animals (control: 137 ± 3 L-NAME: 157 ± 7, L-NAME + NO2 (-): 136 ± 5 mm Hg). Also, NO2 (-) infusion significantly increased VC when compared to L-NAME (P < 0.03), ultimately negating any significant differences from control animals (control: 0.78 ± 0.05, L-NAME: 0.57 ± 0.03, L-NAME + NO2 (-); 0.69 ± 0.04 mL min(-1) 100 g(-1) mm Hg(-1)) with no apparent fiber-type preferential effect. Overall, hindlimb BF was decreased significantly by L-NAME; however, in L-NAME + NO2 (-), BF improved to a level not significantly different from healthy controls (control: 108 ± 8, L-NAME: 88 ± 3, L-NAME + NO2 (-): 94 ± 6 mL min(-1) 100 g(-1), P = 0.38 L-NAME vs L-NAME + NO2 (-)). Individuals with diseases that impair NOS activity, and thus vascular function, may benefit from a NO2 (-)-based therapy in which NO bioavailability is elevated in an NOS-independent manner.en_GB
dc.description.sponsorshipThe author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: These experiments were funded by a Kansas State University SMILE award to TIM, and American Heart Association Midwest Affiliate (10GRNT4350011) and NIH (HL-108328) awards to DCP.en_GB
dc.identifier.citationVol. 21, pp. 201 - 208en_GB
dc.identifier.doi10.1177/1074248415599061
dc.identifier.other1074248415599061
dc.identifier.urihttp://hdl.handle.net/10871/20346
dc.language.isoenen_GB
dc.publisherSAGE Publicationsen_GB
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/26272082en_GB
dc.subjectblood flowen_GB
dc.subjectnitrateen_GB
dc.subjectnitric oxideen_GB
dc.subjectvascular controlen_GB
dc.titleSkeletal muscle vascular control during exercise: impact of nitrite infusion during nitric oxide synthase inhibition in healthy rats.en_GB
dc.typeArticleen_GB
dc.date.available2016-03-01T15:27:37Z
dc.identifier.issn1074-2484
exeter.place-of-publicationUnited States
dc.descriptionThis is the author accepted manuscript. The final version is available from Sage via the DOI in this recorden_GB
dc.identifier.journalJournal of Cardiovascular Pharmacology and Therapeuticsen_GB
dc.identifier.pmid26272082


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