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
Home Search Quick Search Advanced Fulltext Browse Collections Persons My eDoc Session History Login Name: Password: Documentation Help 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 Volume: 27 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 Identifiers: URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=... 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.