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1 Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
2 Department of Pharmacology, University of Pennsylvania, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: jefaber{at}med.unc.edu.
Catecholamine stimulation of 
1-adrenoceptors exerts growth factor-like activity, mediated by generation of reactive oxygen species (ROS), on arterial smooth muscle cells and adventitial fibroblasts, and contributes to hypertrophy and hyperplasia in models of vascular injury and disease. Adrenergic trophic activity also contributes to flow-mediated positive arterial remodeling by augmenting proliferation and leukocyte accumulation. To further examine this concept, we studied whether catecholamines contribute to collateral growth and angiogenesis in hind limb insufficiency. Support for this hypothesis includes the above studies, evidence that ischemia augments norepinephrine release from sympathetic nerves, and proposed involvement of ROS in angiogenesis and collateral growth. Mice deficient in catecholamine synthesis (dopamine 
-hydroxylase-/-, DBH-/-) were studied. Three weeks after femoral artery ligation, increases in adductor muscle perfusion were similar in DBH-/- and wild-type, whereas recovery of plantar perfusion and calf microsphere flow were attenuated although non-significantly. Pre-existing collaterals in adductor of wild-type evidenced increases in lumen diameter (60%) and medial and adventitial thickness (57 and 119%) (values here and below are p<0.05). Lumen diameter increased similarly in DBH-/- (52%), however increases in medial and adventitial thicknesses were reduced (30 and 65%). Leukocyte accumulation in the adventitia/peri-adventitia of collaterals was 39% less in DBH-/-. Increased density of -smooth muscle actin-positive vessels in wild-type adductor (45%) was inhibited in DBH-/- (2%). Although both groups experienced similar atrophy in gastrocnemius (~22%), the increase in capillary-to-muscle fiber ratio in wild-type (21%) was inhibited in DBH-/- (7%). These data suggest that catecholamines may contribute to collateral growth and angiogenesis in tissue ischemia.
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