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1 Department of Biomedical Sciences, College of Veterinary Medicine, 2 Department of Physiology, College of Medicine, and 3 Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211-5120
Nitric oxide (NO) has been implicated in both
collateral expansion (arteriogenesis) and capillary growth
(angiogenesis). Exercise training increases collateral-dependent blood
flow to tissues at risk of ischemia and enhances capillarity in
active skeletal muscle. Exercise also acutely elevates NO. Thus we
assessed the role of NO in training-induced arteriogenesis and
angiogenesis. These studies utilized a rat model of peripheral vascular
disease (bilateral femoral artery ligation). Untreated rats (control) and rats treated with the NO synthase inhibitor
N
-nitro-L-arginine methyl ester
(L-NAME; 65-70
mg · kg
1 · day1, via
drinking water) were divided into sedentary or exercise-trained subgroups. After ~3 wk, L-NAME treatment had elevated
preexercise mean arterial pressure ~39-58%, confirming NO
synthesis inhibition. The training program (treadmill exercise twice
per day, 20-25 m/min, 15% grade, ~18 days) increased
collateral-dependent blood flow to the distal hindlimb, with the
greatest increase (~59%) in the calf (P < 0.001).
This increase was inhibited by L-NAME. In contrast, the
training-induced increase in muscle capillarity was not blocked by
L-NAME. Thus arteriogenesis and angiogenesis appear to
differ in their requirement for NO.
N-nitro-L-arginine methyl
ester; exercise training; capillaries; arterioles; nitric oxide
synthase
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