{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T20:26:22Z","timestamp":1760646382363,"version":"3.37.3"},"reference-count":52,"publisher":"American Physiological Society","issue":"8","funder":[{"name":"SMILE"},{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["10GRNT4350011"],"award-info":[{"award-number":["10GRNT4350011"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000009","name":"Foundation for the National Institutes of Health (FNIH)","doi-asserted-by":"publisher","award":["HL-108328"],"award-info":[{"award-number":["HL-108328"]}],"id":[{"id":"10.13039\/100000009","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:p> Chronic heart failure (CHF) reduces nitric oxide (NO) bioavailability and impairs skeletal muscle vascular control during exercise. Reduction of NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> to NO may impact exercise-induced hyperemia, particularly in muscles with pathologically reduced O<jats:sub>2<\/jats:sub> delivery. We tested the hypothesis that NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> infusion would increase exercising skeletal muscle blood flow (BF) and vascular conductance (VC) in CHF rats with a preferential effect in muscles composed primarily of type IIb + IId\/x fibers. CHF (coronary artery ligation) was induced in adult male Sprague-Dawley rats. After a &gt;21-day recovery, mean arterial pressure (MAP; carotid artery catheter) and skeletal muscle BF (radiolabeled microspheres) were measured during treadmill exercise (20 m\/min, 5% incline) with and without NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> infusion. The myocardial infarct size (35 \u00b1 3%) indicated moderate CHF. NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> infusion increased total hindlimb skeletal muscle VC (CHF: 0.85 \u00b1 0.09 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g<jats:sup>\u22121<\/jats:sup>\u00b7mmHg<jats:sup>\u22121<\/jats:sup> and CHF + NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>: 0.93 \u00b1 0.09 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g<jats:sup>\u22121<\/jats:sup>\u00b7mmHg<jats:sup>\u22121<\/jats:sup>, P &lt; 0.05) without changing MAP (CHF: 123 \u00b1 4 mmHg and CHF + NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>: 120 \u00b1 4 mmHg, P = 0.17). Total hindlimb skeletal muscle BF was not significantly different (CHF: 102 \u00b1 7 and CHF + NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>: 109 \u00b1 7 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g<jats:sup>\u22121<\/jats:sup> ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g<jats:sup>\u22121<\/jats:sup>, P &gt; 0.05). BF increased in 6 (\u223c21%) and VC in 8 (\u223c29%) of the 28 individual muscles and muscle parts. Muscles and muscle portions exhibiting greater BF and VC after NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> infusion comprised \u226563% type IIb + IId\/x muscle fibers. These data demonstrate that NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> infusion can augment skeletal muscle vascular control during exercise in CHF rats. Given the targeted effects shown herein, a NO<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>-based therapy may provide an attractive \u201cneeds-based\u201d approach for treatment of the vascular dysfunction in CHF. <\/jats:p>","DOI":"10.1152\/ajpheart.00421.2015","type":"journal-article","created":{"date-parts":[[2015,9,14]],"date-time":"2015-09-14T21:50:13Z","timestamp":1442267413000},"page":"H1354-H1360","source":"Crossref","is-referenced-by-count":16,"title":["Effects of nitrite infusion on skeletal muscle vascular control during exercise in rats with chronic heart failure"],"prefix":"10.1152","volume":"309","author":[{"given":"Angela A.","family":"Glean","sequence":"first","affiliation":[{"name":"Department of Kinesiology, Kansas State University, Manhattan, Kansas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Scott K.","family":"Ferguson","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clark T.","family":"Holdsworth","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Trenton D.","family":"Colburn","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, Kansas State University, Manhattan, Kansas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer L.","family":"Wright","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alex J.","family":"Fees","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karen 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