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1 Biomedical Sciences, College of Veterinary Medicine, and Physiology, College of Medicine, and Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri 65211; and 2 Scios Incorporated, Sunnyvale, California 94086
The angiogenic
proteins basic fibroblast growth factor (bFGF; FGF-2) and vascular
endothelial growth factor 121 (VEGF121) are each able to
enhance the collateral-dependent blood flow after bilateral femoral
artery ligation in rats. To study the effect of nitric oxide (NO)
synthase (NOS) inhibition on bFGF- or VEGF121-induced blood
flow expansion, the femoral arteries of male Sprague-Dawley rats were
ligated bilaterally, and the animals were given tap water
[non-NG-nitro-L-arginine methyl
ester (L-NAME) group; n = 36] or water that contained L-NAME (L-NAME group; 2 mg/ml,
n = 36). Animals from each group were further divided
into three subgroups: vehicle (n = 12), bFGF (5 µg · kg
1 · day1,
n = 12), or VEGF121 (10 µg · kg1 · day1,
n = 12). Growth factors were delivered via
intra-arterial infusion with osmotic pumps over days
1-14. On day 16, after a 2-day delay to permit
clearance of bFGF and VEGF from the circulation, maximal collateral
blood flow was determined by 85Sr- and
141Ce-labeled microspheres during treadmill running.
L-NAME (~137 mg · kg1 · day1) for 18 days increased systemic blood pressure (~26%, P < 0.001). In the absence of L-NAME, collateral-dependent
blood flows to the calf muscles were greater in the
VEGF121- and bFGF-treated subgroups (85 ± 4.5 and
80 ± 2.9 ml · min1 · 100 g1, respectively) than in the vehicle subgroup (49 ± 3.0 ml · min1 · 100 g1,
P < 0.001). In the presence of NOS inhibition by
L-NAME, blood flows to the calf muscles were essentially
equivalent among the three subgroups (54 ± 3.0, 56 ± 5.1, and 47 ± 2.0 ml · min1 · 100 g1 in the bFGF-, VEGF121-, and
vehicle-treated subgroups, respectively) and were not different from
the blood flow in the non-L-NAME vehicle subgroup. Our
results therefore indicate that normal NO production is essential for
the enhanced vascular remodeling induced by exogenous bFGF or
VEGF121 in this rat model of experimental peripheral
arterial insufficiency. These results imply that a blunted endothelial NO production could temper vascular remodeling in response to these
angiogenic growth factors.
angiogenesis; vascular remodeling; peripheral arterial insufficiency; microsphere; rat
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