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            <funder>This study was supported by Association Française contre les Myopathies JBS and LH N. 13031, and SB N. 13802, 14389, 15208) and by the Ministère de l'Agriculture et de l'Alimentation (France).</funder>
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              <idno type="pubmed">22193759</idno>
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                <term xml:lang="en">Duchenne muscular dystrophic cardiomyopathy</term>
                <term xml:lang="en">endothelial dysfunction</term>
                <term xml:lang="en">endothelial nitric oxide synthase</term>
                <term xml:lang="en">neuronal nitric oxide synthase</term>
                <term xml:lang="en">bradykinin</term>
              </keywords>
              <classCode scheme="mesh">Animals</classCode>
              <classCode scheme="mesh">Blood Pressure</classCode>
              <classCode scheme="mesh">Nitric Oxide Synthase Type I</classCode>
              <classCode scheme="mesh">Nitric Oxide Synthase Type III</classCode>
              <classCode scheme="mesh">Ventricular Dysfunction, Left</classCode>
              <classCode scheme="mesh">Bradykinin</classCode>
              <classCode scheme="mesh">Carotid Arteries</classCode>
              <classCode scheme="mesh">Cyclic GMP</classCode>
              <classCode scheme="mesh">Disease Models, Animal</classCode>
              <classCode scheme="mesh">Dogs</classCode>
              <classCode scheme="mesh">Endothelium, Vascular</classCode>
              <classCode scheme="mesh">Muscular Dystrophy, Duchenne</classCode>
              <classCode scheme="mesh">Nitric Oxide</classCode>
              <classCode scheme="halDomain" n="sdv.bbm">Life Sciences [q-bio]/Biochemistry, Molecular Biology</classCode>
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              <p>Little is known about the vascular function and expression of endothelial and neuronal nitric oxide synthases (eNOS and nNOS) in Duchenne muscular dystrophy (DMD). Bradykinin is involved in the regulation of eNOS expression induced by angiotensin-converting enzyme inhibitors. We characterized the vascular function and eNOS and nNOS expression in a canine model of DMD and evaluated the effects of chronic bradykinin treatment. Vascular function was examined in conscious golden retriever muscular dystrophy (GRMD) dogs with left ventricular dysfunction (measured by echocardiography) and in isolated coronary arteries. eNOS and nNOS proteins in carotid arteries were measured by western blot and cyclic guanosine monophosphate (cGMP) content was analyzed by radioimmunoassay. Compared with controls, GRMD dogs had an impaired vasodilator response to acetylcholine. In isolated coronary artery, acetylcholine-elicited relaxation was nearly absent in placebo-treated GRMD dogs. This was explained by reduced nNOS and eNOS proteins and cGMP content in arterial tissues. Chronic bradykinin infusion (1 μg/min, 4 weeks) restored in vivo and in vitro vascular response to acetylcholine to the level of control dogs. This effect was NO-mediated through upregulation of eNOS and nNOS expression. In conclusion, this study is the first to demonstrate that DMD is associated with NO-mediated vascular endothelial dysfunction linked to an altered expression of eNOS and nNOS, which can be overcome by bradykinin.</p>
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