dc.contributor.author | Ferguson, SK | |
dc.contributor.author | Glean, AA | |
dc.contributor.author | Holdsworth, CT | |
dc.contributor.author | Wright, JL | |
dc.contributor.author | Fees, AJ | |
dc.contributor.author | Colburn, TD | |
dc.contributor.author | Stabler, T | |
dc.contributor.author | Allen, JD | |
dc.contributor.author | Jones, AM | |
dc.contributor.author | Musch, TI | |
dc.contributor.author | Poole, DC | |
dc.date.accessioned | 2016-03-01T15:27:37Z | |
dc.date.issued | 2016-03 | |
dc.description.abstract | The 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.sponsorship | The 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.citation | Vol. 21, pp. 201 - 208 | en_GB |
dc.identifier.doi | 10.1177/1074248415599061 | |
dc.identifier.other | 1074248415599061 | |
dc.identifier.uri | http://hdl.handle.net/10871/20346 | |
dc.language.iso | en | en_GB |
dc.publisher | SAGE Publications | en_GB |
dc.relation.url | http://www.ncbi.nlm.nih.gov/pubmed/26272082 | en_GB |
dc.subject | blood flow | en_GB |
dc.subject | nitrate | en_GB |
dc.subject | nitric oxide | en_GB |
dc.subject | vascular control | en_GB |
dc.title | Skeletal muscle vascular control during exercise: impact of nitrite infusion during nitric oxide synthase inhibition in healthy rats. | en_GB |
dc.type | Article | en_GB |
dc.date.available | 2016-03-01T15:27:37Z | |
dc.identifier.issn | 1074-2484 | |
exeter.place-of-publication | United States | |
dc.description | This is the author accepted manuscript. The final version is available from Sage via the DOI in this record | en_GB |
dc.identifier.journal | Journal of Cardiovascular Pharmacology and Therapeutics | en_GB |
dc.identifier.pmid | 26272082 | |