{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T01:41:02Z","timestamp":1792374062133,"version":"4.4.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[1999,4,16]]},"abstract":"<jats:p><jats:italic>Abstract<\/jats:italic>\u2014Our objective was to determine the precise role of endothelial nitric oxide synthase (eNOS) as a modulator of cardiac O<jats:sub>2<\/jats:sub>consumption and to further examine the role of nitric oxide (NO) in the control of mitochondrial respiration. Left ventricle O<jats:sub>2<\/jats:sub>consumption in mice with defects in the expression of eNOS [eNOS (\u2212\/\u2212)] and inducible NOS [iNOS (\u2212\/\u2212)] was measured with a Clark-type O<jats:sub>2<\/jats:sub>electrode. The rate of decreases in O<jats:sub>2<\/jats:sub>concentration was expressed as a percentage of the baseline. Baseline O<jats:sub>2<\/jats:sub>consumption was not significantly different between groups of mice. Bradykinin (10<jats:sup>\u22124<\/jats:sup>mol\/L) induced significant decreases in O<jats:sub>2<\/jats:sub>consumption in tissues taken from iNOS (\u2212\/\u2212) (\u221228\u00b14%), wild-type eNOS (+\/+) (\u221222\u00b14%), and heterozygous eNOS(+\/\u2212) (\u221222\u00b15%) but not homozygous eNOS (\u2212\/\u2212) (\u22123\u00b14%) mice. Responses to bradykinin in iNOS (\u2212\/\u2212) and both wild-type and heterozygous eNOS mice were attenuated after NOS blockade with<jats:italic>N<\/jats:italic>-nitro-<jats:sc>l<\/jats:sc>-arginine methyl ester (L-NAME) (\u22122\u00b15%, \u22123\u00b12%, and \u22126\u00b15%, respectively,<jats:italic>P<\/jats:italic>&lt;0.05). In contrast,<jats:italic>S<\/jats:italic>-nitroso-<jats:italic>N<\/jats:italic>-acetyl-penicillamine (SNAP, 10<jats:sup>\u22124<\/jats:sup>mol\/L), which releases NO spontaneously, induced decreases in myocardial O<jats:sub>2<\/jats:sub>consumption in all groups of mice, and such responses were not affected by L-NAME. In addition, pretreatment with bacterial endotoxin elicited a reduction in basal O<jats:sub>2<\/jats:sub>consumption in tissues taken from normal but not iNOS (\u2212\/\u2212)\u2013deficient mice. Our results indicate that the pivotal role of eNOS in the control of myocardial O<jats:sub>2<\/jats:sub>consumption and modulation of mitochondrial respiration by NO may have an important role in pathological conditions such as endotoxemia in which the production of NO is altered.<\/jats:p>","DOI":"10.1161\/01.res.84.7.840","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:47:05Z","timestamp":1339462025000},"page":"840-845","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":130,"title":["Endogenous Endothelial Nitric Oxide Synthase\u2013Derived Nitric Oxide Is a Physiological Regulator of Myocardial Oxygen Consumption"],"prefix":"10.1161","volume":"84","author":[{"given":"Kit E.","family":"Loke","sequence":"first","affiliation":[{"name":"From the Departments of Physiology (K.E.L., P.I.M., J.M.T., C.I.T., G.K., M.S.W., T.H.H.) and Pathology (C.J. Smith, C.J. Stackpole), New York Medical College, Valhalla, NY; Division of Hypertension and Vascular Research (E.G.S.), Henry Ford Hospital, Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick I.","family":"McConnell","sequence":"additional","affiliation":[{"name":"From the Departments of Physiology (K.E.L., P.I.M., J.M.T., C.I.T., G.K., M.S.W., T.H.H.) and Pathology (C.J. Smith, C.J. Stackpole), New York Medical College, Valhalla, NY; Division of Hypertension and Vascular Research (E.G.S.), Henry Ford Hospital, Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua M.","family":"Tuzman","sequence":"additional","affiliation":[{"name":"From the Departments of Physiology (K.E.L., P.I.M., J.M.T., C.I.T., G.K., M.S.W., T.H.H.) and Pathology (C.J. Smith, C.J. 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