on June 7, 2007
Published online before print June 7, 2007, doi: 10.1161/ATVBAHA.107.145375
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Submitted on May 30, 2006
Accepted on April 20, 2007
Endothelial Nitric Oxide Synthase Activity Is Essential for Vasodilation During Blood Flow Recovery but not for Arteriogenesis
Barend Mees *;
From the Department of Experimental Cardiology (S.W., E.N., S.T., S.M., S.K., M.H., W.S.), Max-Planck-Institute for Heart & Lung Research, Bad Nauheim, Germany; and the Departments of Cell Biology & Genetics (B.M., R.v.H., R.d.C.) and Vascular Surgery (B.M., R.d.C.), Erasmus University MC, Rotterdam, The Netherlands.
* To whom correspondence should be addressed. E-mail: b.mees{at}erasmusmc.nl.
Objective--Arteriogenesis is the major mechanism of vascular growth, which is able to compensate for blood flow deficiency after arterial occlusion. Endothelial nitric oxide synthase (eNOS) activity is essential for neovascularization, however its specific role in arteriogenesis remains unclear. We studied the role of eNOS in arteriogenesis using 3 mouse strains with different eNOS expression.
Methods and Results--Distal femoral artery ligation was performed in eNOS-overexpressing mice (eNOStg), eNOS-deficient (eNOS-/-) mice, and wild-type (WT) controls. Tissue perfusion and collateral-dependent blood flow were significantly increased in eNOStg mice compared with WT only immediately after ligation. In eNOS-/- mice, although tissue perfusion remained significantly decreased, collateral-dependent blood flow was only decreased until day 7, suggesting normal, perhaps delayed collateral growth. Histology confirmed no differences in collateral arteries of eNOStg, eNOS-/-, and WT mice at 1 and 3 weeks. Administration of an NO donor induced vasodilation in collateral arteries of eNOS-/- mice, but not in WT, identifying the inability to vasodilate collateral arteries as main cause of impaired blood flow recovery in eNOS-/- mice.
Conclusions--This study demonstrates that eNOS activity is crucial for NO-mediated vasodilation of peripheral collateral vessels after arterial occlusion but not for collateral artery growth.
Key words: endothelial nitric oxide synthase • arteriogenesis • mouse • hind limb • vasodilation
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