{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T05:46:15Z","timestamp":1715579175613},"reference-count":29,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2005,2]]},"abstract":"<jats:p>Exogenous nitric oxide (NO) suppresses endothelium-derived NO production. We were interested in determining whether this is also the case in flow-induced endothelium-derived NO production. If so, then is the mechanism because of intracellular depletion of tetrahydrobiopterin [BH<jats:sub>4<\/jats:sub>; a cofactor of NO synthase (NOS)], which results in superoxide production by uncoupled NOS? Isolated canine femoral arteries were perfused with 100 \u03bcM S-nitroso- N-acetylpenicillamine (SNAP; an NO donor) and\/or 64 \u03bcM BH<jats:sub>4<\/jats:sub>. Perfusion of SNAP suppressed flow-induced NO production, which was evaluated as a change in the slope of the linear relationship between perfusion rate and NO production rate ( P &lt; 0.02 vs. control; n = 7). Subsequent BH<jats:sub>4<\/jats:sub>perfusion returned the slope to the control level. Concomitant perfusion of SNAP and BH<jats:sub>4<\/jats:sub>retained the control-level NO production ( n = 7). Concomitant perfusion of SNAP and 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron; 1 mM; a membrane-permeable superoxide scavenger) also retained the control-level NO production ( n = 7), whereas perfusion of Tiron after SNAP could not return the NO production to the control level ( P &lt; 0.02 vs. control; n = 7). We also found a significant decrease in BH<jats:sub>4<\/jats:sub>concentration in the endothelial cells after SNAP perfusion. In conclusion, these results indicate that exogenous NO suppresses the flow-induced, endothelium-derived NO production by superoxide released from uncoupled NOS because of intracellular BH<jats:sub>4<\/jats:sub>depletion.<\/jats:p>","DOI":"10.1152\/ajpheart.00408.2004","type":"journal-article","created":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:24:14Z","timestamp":1097195054000},"page":"H553-H558","source":"Crossref","is-referenced-by-count":9,"title":["Exogenous NO suppresses flow-induced endothelium-derived NO production because of depletion of tetrahydrobiopterin"],"prefix":"10.1152","volume":"288","author":[{"given":"Seiichi","family":"Mochizuki","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pieter","family":"Sipkema","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masami","family":"Goto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Osamu","family":"Hiramatsu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Nakamoto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eiji","family":"Toyota","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tatsuya","family":"Kajita","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fumiyuki","family":"Shigeto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toyotaka","family":"Yada","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuo","family":"Ogasawara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fumihiko","family":"Kajiya","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.5.H1849"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.73.5.808"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.271.5.H1988"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1159\/000025568"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(99)00134-0"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1002\/biof.5520060215"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1994.tb19972.x"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Griscavage JM, Fukuto JM, Komori Y, and Ignarro LJ.Nitric oxide inhibits neuronal nitric oxide synthase by interacting with the heme prosthetic group. 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