{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,11]],"date-time":"2026-05-11T21:55:52Z","timestamp":1778536552675,"version":"3.51.4"},"reference-count":36,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2002,10,18]],"date-time":"2002-10-18T00:00:00Z","timestamp":1034899200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2002,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Nitric oxide (NO) has multiple important actions that contribute to the maintenance of vascular homeostasis. NO is synthesized by three different isoforms of NO synthase (NOS), all of which have been reported to be expressed in human atherosclerotic vascular lesions. Although the regulatory roles of endothelial NOS (eNOS) and inducible NOS (iNOS) on the development of atherosclerosis have been described, little is known about the role of neuronal NOS (nNOS). Here, we show that nNOS also exerts important vasculoprotective effects\n                    <jats:italic>in vivo<\/jats:italic>\n                    . In a carotid artery ligation model, nNOS gene\u2010deficient (nNOS\u2010KO) mice exhibited accelerated neointimal formation and constrictive vascular remodeling caused by blood flow disruption. In a rat balloon injury model, the selective inhibition of nNOS activity potently enhanced vasoconstrictor responses to a variety of calcium\u2010mobilizing stimuli, suppressed tissue cGMP concentrations, a marker of vascular NO production, and exacerbated neointimal formation. In both models, nNOS was absent before injury and was up\u2010regulated only after the injury, and was predominantly expressed in the neointima and medial smooth muscle cells. These results provide the first direct evidence that nNOS plays important roles in suppressing arteriosclerotic vascular lesion formation\n                    <jats:italic>in vivo<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1096\/fj.02-0155fje","type":"journal-article","created":{"date-parts":[[2002,12,5]],"date-time":"2002-12-05T12:43:29Z","timestamp":1039092209000},"page":"1994-1996","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":84,"title":["Vasculoprotective Roles of Neuronal Nitric Oxide Synthase"],"prefix":"10.1096","volume":"16","author":[{"given":"Tsuyoshi","family":"Morishita","sequence":"first","affiliation":[{"name":"Second Department of Internal Medicine University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masato","family":"Tsutsui","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"},{"name":"Department of Pharmacology University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroaki","family":"Shimokawa","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine Kyushu University Graduate School of Medical Sciences  Fukuoka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masataka","family":"Horiuchi","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akihide","family":"Tanimoto","sequence":"additional","affiliation":[{"name":"Department of Pathology and Cell Biology University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Osamu","family":"Suda","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiromi","family":"Tasaki","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul L","family":"Huang","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center Massachusetts General Hospital, Harvard Medical School  Boston Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuyuki","family":"Sasaguri","sequence":"additional","affiliation":[{"name":"Department of Pathology and Cell Biology University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuyuki","family":"Yanagihara","sequence":"additional","affiliation":[{"name":"Department of Pharmacology University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuhide","family":"Nakashima","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine University of Occupational and Environmental Health, School of Medicine  Kitakyushu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2002,10,18]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.63.070194.001135"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119751"},{"key":"e_1_2_6_4_1","volume-title":"The Endothelium: Modulator of Cardiovascular Function","author":"Luscher T. 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