{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T17:38:16Z","timestamp":1760204296384},"reference-count":26,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2010,1,26]],"date-time":"2010-01-26T00:00:00Z","timestamp":1264464000000},"content-version":"vor","delay-in-days":5170,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Microcirculation"],"published-print":{"date-parts":[[1995,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:bold>Objective<\/jats:bold>: This study was designed to investigate the role of dietary copper in nitric oxide\u2010mediated arteriolar dilation.<\/jats:p><jats:p><jats:bold>Methods<\/jats:bold>: Male weanling Sprague\u2014Dawley rats were fed a purified diet that was either copper\u2010adequate (6.0 \u03bcg Cu per g diet) or copper\u2010deficient (0.3 \u03bcg Cu per g diet) for a period of 4 weeks. Each rat was anesthetized with pentobarbital and its cremaster muscle was positioned in a Krebs'\u2010fdled bath to which graded concentrations of vasoactive agents were added. In the first series, responses to norepineph\u2010rine (NE 10<jats:sup>\u22129<\/jats:sup>\u201010<jats:sup>\u22126<\/jats:sup> M) and acetylcholine (ACH 10<jats:sup>\u22127<\/jats:sup>\u201010<jats:sup>\u22124<\/jats:sup> M) were compared in third\u2010order arterioles. Second, the dilator response to 10<jats:sup>\u22125<\/jats:sup> M ACH in the absence and presence of 240 U\/ml Cu, Zn\u2010superoxide dismutase (SOD) was determined. Third, arteriolar dilation was determined in response to NO\u2010independent stimulation of soluble guanylate cyclase with hydrogen peroxide (10<jats:sup>\u22127<\/jats:sup>\u201010<jats:sup>\u22125<\/jats:sup> M) and to dibutyryl cGMP (10<jats:sup>\u22126<\/jats:sup>\u201010<jats:sup>\u22124<\/jats:sup> M), dibutyryl cAMP (10<jats:sup>\u22126<\/jats:sup>\u201010<jats:sup>\u22124<\/jats:sup> M), and papaverine (10<jats:sup>\u22124<\/jats:sup>M).<\/jats:p><jats:p><jats:bold>Results<\/jats:bold>: The arteriole constrictor response to NE and the dilator response to hydrogen peroxide, dibutyryl cGMP and cAMP, and papaverine were not different between the dietary groups. Copper deficiency attenuated the ACH\u2010induced dilation, but the response was restored in the presence of SOD.<\/jats:p><jats:p><jats:bold>Conclusions<\/jats:bold>: The inactivation of cytosolic Cu, Zn\u2010SOD by restriction of dietary copper results in the depression of NO\u2010mediated vascular smooth\u2010muscle relaxation probably by interaction of NO with superoxide.<\/jats:p>","DOI":"10.3109\/10739689509148281","type":"journal-article","created":{"date-parts":[[2008,4,23]],"date-time":"2008-04-23T22:26:39Z","timestamp":1208989599000},"page":"371-376","source":"Crossref","is-referenced-by-count":27,"title":["A Role for Dietary Copper in Nitric Oxide\u2010Mediated Vasodilation"],"prefix":"10.1111","volume":"2","author":[{"given":"Dale A.","family":"Schuschke","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jack 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