Please note that eDoc will be permanently shut down in the first quarter of 2021!      Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Quick Search
My eDoc
Session History
Support Wiki
Direct access to
document ID:

          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Publikationen des W. G. Kerckhoff-Instituts     Display Documents

ID: 354752.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Publikationen des W. G. Kerckhoff-Instituts
Endothelial nitric oxide synthase activity is essential for vasodilation during blood flow recovery but not for arteriogenesis
Authors:Mees, B.; Wagner, S.; Ninci, E.; Tribulova, S.; Martin, S.; van Haperen, R.; Kostin, S.; Heil, M.; de Crom, R.; Schaper, W.
Date of Publication (YYYY-MM-DD):2007-09
Journal Abbrev.:Arterioscler Thromb Vasc Biol
Issue / Number:9
Start Page:1926
End Page:1933
Audience:Not Specified
Abstract / Description: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.
Free Keywords:Animals; Collateral Circulation/physiology; Disease Models, Animal; Femoral Artery/injuries; Mice; Mice, Transgenic; Neovascularization, Physiologic/*physiology; Nitric Oxide/*metabolism; Nitric Oxide Synthase Type II/genetics/*metabolism; Vasodilation/*physiology
External Publication Status:published
Document Type:Article
Communicated by:N. N.
Affiliations:MPI für physiologische und klinische Forschung
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.