NO produced by eNOS plays important roles in the cardiovascular system. Alterations in eNOS activity
and expression occur in various cardiovascular disorders and eNOS constitutes a therapeutic target. In addition
to posttranslational modifications of eNOS that affect eNOS activity, transcriptional and post-transcriptional
regulation of eNOS expression also controls eNOS-derived NO production. Bradykinin is an important determinant
of vascular function and participates in the regulation of eNOS activity and expression. A number of currently
used drugs or investigational molecules targeting specific ion channels, enzymes or receptors, including
dihydropyridine calcium channel blockers, angiotensin-converting enzyme inhibitors, statins, AT1 receptor
blockers and angiotensin-(1-7), increase eNOS expression and activity. In this context, activation of bradykinin
B2 receptors appears to be a common step for these drugs to promote eNOS expression, which certainly contributes
to their therapeutic actions.
Keywords: Angiotensin-converting enzyme inhibitors, angiotensin-(1-7), AT1 receptor blockers, bradykinin, dihydropyridine calcium channel
blockers, statins, endothelial nitric oxide synthase, nitric oxide, transcriptional and posttranscriptional regulation.
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