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1 Cell and Molecular Physiology, University of North Carolina, Chapel Hill, NC, USA
2 Molecular and Cellular Pharmacology, National Research Institute, Tokyo, Japan
3 Genomic Drug Discovery Science, Kyoto University, Kyoto, Japan
4 Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
* To whom correspondence should be addressed. E-mail: jefaber{at}med.unc.edu.
Alpha1-adrenoceptor (AR) stimulation 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 the murine carotid artery, these effects are mediated by alpha1B-ARs, whereas alpha1D-ARs mediate contraction and alpha1A-ARs are not expressed. Herein, we examined whether catecholamines also contribute to arterial wall growth in a non-injury model, ie, flow-mediated remodeling. In wildtype or mice deficient in norepinephrine and epinephrine synthesis [dopamine beta-hydroxylase knockout (DBH-KO)], all distal branches of the left carotid (LC) except the thyroid artery were ligated to reduce flow in the LC and increase flow in the right carotid (RC). Twenty-one days later, negative hypertrophic remodeling of LC [ie, -20%** (decrease) in lumen area, -2% in circumference of the external elastic lamina (CEEL), +98%** (increase) in thickness of intima-media and +71%** for adventitia; **p<0.01 vs. sham-ligation] and positive eutrophic remodeling of RC [+23%** in lumen area, +11%** in CEEL] were inhibited in DBH-KOs [LC: +10% intima-media and +3% adventitia; RC: +9% lumen area and +3% CEEL]. This inhibition was associated with reduced proliferation in RC and reduced apoptosis and leukocyte accumulation in RC and LC, when examined 5 days after ligation. Carotid remodeling in alpha1D-AR-KOs evidenced little or no inhibition, suggesting dependence on alpha1B-ARs. These findings suggest that catecholamine-induced trophic activity contributes to both flow-mediated negative remodeling and adaptive positive arterial remodeling.
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