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Am J Physiol Heart Circ Physiol 281: H2528-H2538, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 6, H2528-H2538, December 2001

Arteriogenesis and angiogenesis in rat ischemic hindlimb: role of nitric oxide

Pamela G. Lloyd1, Hsiao T. Yang1, and Ronald L. Terjung1,2,3

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 Nomega -nitro-L-arginine methyl ester (L-NAME; 65-70 mg · kg-1 · day-1, 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.

Nomega -nitro-L-arginine methyl ester; exercise training; capillaries; arterioles; nitric oxide synthase


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