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Yang, H T.1
1Biomedical Sciences, University of Missouri, Columbia MO
Vascular remodeling includes two major processes: arteriogenesis (collateral arterial expansion) and angiogenesis (new capillary growth). Both of the processes are thought to be precisely regulated by angiogenic factors induced by shear stress, hypoxia, inflammation, and muscle contractions. In animals with femoral artery occlusion, exercise training enhances collateral dependent blood flow (BF) by enlarging of collateral arteries, and increases tissue O2 exchange capacity by increasing capillarity in the active skeletal muscles. Since nitric oxide (NO) can be a part of the VEGF signaling pathway, we hypothesized that NO would be required for both of the remodeling processes. The role of NO was assessed by chronic inhibition of NO synthase (NOS) with L-NAME. The effectiveness of NOS inhibition was confirmed by ∼50% increase in mean blood pressure (p < 0.01). Inhibition of normal NO production eliminated the ∼75% exercise-induced increase in collateral conductance (p < 0.001). However, the exercise training-induced increase in muscle capillarity (capillary contacts per fiber) was not blocked by L-NAME. These findings suggest that arteriogenesis and angiogenesis are regulated differently in response to exercise training and that the requirement for NO in vascular remodeling is not equivalent in the two processes. Supported by NIH grant HL38387
©2003The American College of Sports Medicine
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