Endogenous catecholamine stimulation of adrenergic receptors contributes to artery growth and remodeling in pathological and adaptive physiological settings. Recently, it has been shown that enforced stem/progenitor cells egress from bone marrow (BM) niches depends critically on the nervous system. In particular, pharmacological or genetic ablation of adrenergic neurotransmission indicates that noradrenalin (NA) signaling controls bone SDF-1 downregulation, and hematopoietic stem cells mobilization. We hypothesized that catecholamines may control vascular progenitor cells mobilization from bone marrow and subsequently trigger post-ischemic neovascularization.Ischemia was induced by right femoral artery ligation in C57Bl6 mice (n=7 per group) treated with or without 6-hydroxydopamin (6-OHDA, 100mg/kg, i.p., 2 days), clenbuterol (2mg/kg, i.p., 5 days), dopamine (DA, 50mg/kg, i.p., 5 days), NA (2.5mg/kg, i.p., 5 days) and eticlopride (10mg/kg, i.p., 5 days). Sympathectomy induced by 6-OHDA led to a decrease in foot perfusion, angiographic score and capillary density by 41.4 % (p