作者: James L. Williams , David Cartland , Arif Hussain , Stuart Egginton
DOI: 10.1113/JPHYSIOL.2005.095596
关键词: Pathology 、 Filopodia 、 Prazosin 、 Enos 、 Biology 、 Skeletal muscle 、 Cell biology 、 Sprouting angiogenesis 、 Nitric oxide 、 Nitroarginine 、 Angiogenesis
摘要: NO plays a role in variety of vitro models angiogenesis, although confounding effects on non-endothelial tissues make its during vivo angiogenesis unclear. We therefore examined the two physiological mouse skeletal muscle: (1) administration prazosin (50 mg l−1) thereby increasing blood flow; and (2) muscle overload from surgical ablation functional synergist. These induce via longitudinal splitting capillary sprouting, respectively. Administration NG-nitro-l-arginine (l-NNA) abolished increase to fibre ratio (C:F) response administration, along with increases luminal filopodia large endothelial vacuoles. l-NNA prevented vacuolisation extirpation, but had no effect abluminal little C:F. Comparison mice lacking (eNOS−/−) neuronal synthase (nNOS−/−) showed that is eNOS-dependent, Western blotting demonstrated an eNOS not inducible NOS (iNOS) expression. data show there are pathways characterised by generated essential sprouting which has important implications for angiogenic therapies target NO.