作者: D. Fukumura , T. Gohongi , A. Kadambi , Y. Izumi , J. Ang
关键词:
摘要: Nitric oxide (NO) plays a critical role in vascular endothelial growth factor (VEGF)-induced angiogenesis and hyperpermeability. However, the relative contribution of different NO synthase (NOS) isoforms to these processes is not known. Here, we evaluated contributions inducible NOS (eNOS iNOS, respectively) permeability VEGF-induced angiogenic vessels. The eNOS was assessed by using an eNOS-deficient mouse, iNOS selective inhibitor [l-N(6)-(1-iminoethyl) lysine, l-NIL] iNOS-deficient mouse. Angiogenesis induced VEGF type I collagen gels placed mouse cranial window. Angiogenesis, vessel diameter, blood flow rate, were proportional levels measured with microelectrodes: Wild-type (WT) > or = WT l-NIL iNOS(-/-) eNOS(-/-) l-NIL. acute increase quiescent vessels also determined eNOS- mice. superfusion significantly increased both mice but These findings suggest that predominant permeability. Thus, modulation activity promising strategy for altering vivo.