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Am J Physiol Heart Circ Physiol (July 1, 2004). doi:10.1152/ajpheart.00290.2004
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Submitted on March 23, 2004
Accepted on June 25, 2004

Gene Deletion of Dopamine {beta}-Hydroxylase and {alpha}1-Adrenoceptors Demonstrates Involvement of Catecholamines in Vascular Remodeling

Hua Zhang1, Susanna Cotecchia2, Steven A. Thomas3, Akito Tanoue4, Gozoh Tsujimoto4, and James E. Faber1*

1 Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, NC, USA
2 Institut de Pharmacologie et Toxicologie, University of Lausanne, Lausanne, Swaziland
3 Department of Pharmacology, University of Pennsylvania, Philadelphia, PA, USA
4 Department of Molecular and Cellular Pharmacology, National Children's Medical Research Center, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: jefaber{at}med.unc.edu.

In vitro studies have shown that stimulation of {alpha}1-adrenoceptors (AR) directly induces proliferation, hypertrophy and migration of arterial smooth muscle cells and adventitial fibroblasts. In vivo studies have confirmed these findings and found that catecholamine trophic activity becomes excessive after experimental balloon injury and contributes to neointimal growth, adventitial thickening and lumen loss. However, past studies have been limited by selectivity of pharmacological agents. The aim of this study was to test the hypothesis that catecholamines contribute to wall hypertrophy after injury, using mice devoid of norepinephrine and epinephrine synthesis [dopamine {beta}-hydroxylase (DBH-/-)] or deficient in the {alpha}1-AR subtypes expressed in murine carotid ({alpha}1B-AR-/- and {alpha}1D-AR-/-). Three weeks after injury of wild-type mice, lumen area and carotid circumference increased significantly, and hypertrophy of media and adventitia was in excess of that needed to restore circumferential wall stress to normal. In DBH-/- and {alpha}1B-AR-/-, increases in lumen area, circumference, and medial and adventitial hypertrophy were reduced by 50-91%, resulting in restoration of wall tension closer to (DBH-/-) or equal to ({alpha}1B-/-) normal. In contrast, in {alpha}1D-AR-/-, increases in lumen area, circumference and wall hypertrophy were unaffected and wall thickening remained in excess of that required to return tension to normal. When examined 5 days after injury, proliferation and leukocyte infiltration were inhibited in DBH-/-. These studies suggest that the trophic effects of catecholamines are mediated primarily by {alpha}1B-ARs in mouse carotid and contribute to hypertrophic growth after vascular injury.




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