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This Article Full Text Full Text (PDF) All Versions of this Article: 289/2/H947    most recent 00952.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (13) Citing Articles via Google Scholar Google Scholar Articles by Chalothorn, D. Articles by Faber, J. E. Search for Related Content PubMed PubMed Citation Articles by Chalothorn, D. Articles by Faber, J. E.

Catecholamines augment collateral vessel growth and angiogenesis in hindlimb ischemia

¹Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina; and ²Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania

Submitted 13 September 2004 ; accepted in final form 7 April 2005

Catecholamine stimulation of ₁-adrenoceptors exerts growth factor-like activity, mediated by generation of reactive oxygen species, 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 hindlimb insufficiency. Support for this hypothesis includes the above-mentioned studies, evidence that ischemia augments norepinephrine release from sympathetic nerves, and proposed involvement of reactive oxygen species in angiogenesis and collateral growth. Mice deficient in catecholamine synthesis [by gene deletion of dopamine -hydroxylase (DBH^–/–)] were studied. At 3 wk after femoral artery ligation, increases in adductor muscle perfusion were similar in DBH^–/– and wild-type mice, whereas recovery of plantar perfusion and calf microsphere flow were attenuated, although not significantly. Preexisting collaterals in adductor of wild-type mice showed increases in lumen diameter (60%) and medial and adventitial thickness (57 and 119%, P < 0.05 here and below). Lumen diameter increased similarly in DBH^–/– mice (52%); however, increases in medial and adventitial thicknesses were reduced (30 and 65%). Leukocyte accumulation in the adventitia/periadventitia of collaterals was 39% less in DBH^–/– mice. Increased density of -smooth muscle actin-positive vessels in wild-type adductor (45%) was inhibited in DBH^–/– mice (2%). Although both groups experienced similar atrophy in the gastrocnemius (22%), the increase in capillary-to-muscle fiber ratio in wild-type mice (21%) was inhibited in DBH^–/– mice (7%). These data suggest that catecholamines may contribute to collateral growth and angiogenesis in tissue ischemia.

dopamine -hydroxylase; arteriogenesis; laser-Doppler imaging

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