Yasunobu Hirata, Daisuke Nagata, Etsu Suzuki, Hiroaki Nishimatsu, Jun-Ichi Suzuki, Ryozo Nagai
Journal: International heart journal 2010;51(1):1-6
PMID: 20145343
Vascular endothelial dysfunction reflected by reduced nitric oxide (NO) availability is certainly the causative factor or promoting mechanism of arteriosclerosis. It is necessary to detect endothelial dysfunction at an early stage using appropriate methods, and to choose a treatment for the recovery of endothelial function. There are nonpharmacological and pharmacological therapies to attain endothelial repair. The former includes body weight reduction, aerobic exercise, and restriction of salt intake, while the latter includes the use of renin-angiotensin system inhibitors, calcium antagonists, some types of beta blockers, statins, erythropoietin, tetrahydrobiopterin, and antioxidants. These therapies are intended to increase NO synthase activity and NO release, inhibit NO degradation, and enhance the activity of endothelial progenitor cells.
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