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Adrenergic catecholamine trophic activity contributes to flow-mediated arterial remodeling

¹Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina; ²Department of Molecular and Cellular Pharmacology, National Research Institute for Child Health and Development, Tokyo; ³Department of Genomic Drug Discovery Science, Kyoto University, Kyoto, Japan; and ⁴Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania

Submitted 8 February 2005 ; accepted in final form 22 March 2005

Stimulation of ₁-adrenoceptors (ARs) induces proliferation, hypertrophy, and migration of vascular smooth muscle cells and adventitial fibroblasts in cell and organ culture. In vivo studies have confirmed this direct trophic action and found that endogenous catecholamines contribute to neointimal formation and wall hypertrophy induced by mechanical injury. In murine carotid artery, these effects are mediated by _1B-ARs, whereas _1D-ARs mediate contraction and _1A-ARs are not expressed. Herein, we examined whether catecholamines also contribute to arterial wall growth in a noninjury model, i.e., flow-mediated remodeling. In wild-type mice or mice deficient in norepinephrine and epinephrine synthesis [dopamine -hydroxylase knockout (DBH-KO)], all distal branches of the left carotid artery (LC) except the thyroid artery were ligated to reduce flow in the LC and increase flow in the right carotid artery (RC). Twenty-one days later, negative hypertrophic remodeling of the LC [i.e., –20% (decrease) in lumen area, –2% in circumference of the external elastic lamina (CEEL), +98% (increase) in thickness of the intima media, and +71% in thickness for adventitia; P < 0.01 vs. sham ligation] and positive eutrophic remodeling of the RC [+23% in lumen area, +11% in CEEL; P < 0.01 vs. sham ligation] were inhibited in DBH-KO mice [LC: +10% intima media and +3% adventitia; RC: +9% lumen area and +3% CEEL]. This inhibition was associated with reduced proliferation in the RC and reduced apoptosis and leukocyte accumulation in the RC and LC when examined 5 days after ligation. Carotid remodeling in _1D-AR-knockout mice evidenced little or no inhibition, which suggests dependence on _1B-ARs. These findings suggest that catecholamine-induced trophic activity contributes to both flow-mediated negative remodeling and adaptive positive arterial remodeling.

dopamine -hydroxylase; carotid; -adrenoceptor; apoptosis; leukocyte accumulation; restenosis

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