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Am J Physiol Heart Circ Physiol 284: H385-H392, 2003. First published September 19, 2002; doi:10.1152/ajpheart.00658.2002
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Vol. 284, Issue 1, H385-H392, January 2003

Systemic alpha 1A-adrenoceptor antagonist inhibits neointimal growth after balloon injury of rat carotid artery

John C. Teeters*, Cauveh Erami*, Hua Zhang, and James E. Faber

Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina, 27599-7545

Previous in vitro and in vivo studies have shown that norepinephrine, acting through alpha 1A-adrenoceptors, stimulates hypertrophy, proliferation, and migration of vascular smooth muscle cells and adventitial fibroblasts and may contribute to neointimal growth, lumen loss, and inward remodeling caused by iatrogenic wall injury and vascular disease. Our present aim was to determine whether intravenous administration of the alpha 1A-adrenoceptor antagonist KMD-3213, at dosages without systemic hemodynamic effects, inhibits wall growth after injury. Inhibition of alpha 1A-adrenoceptors with 12.8 and 32 µg/kg KMD-3213 had no effect on arterial pressure or renal and hindquarter resistances in anesthetized rats. A second group then received carotid balloon injury and continuous intravenous KMD-3213 at 4 and 10 µg · kg-1 · h-1 for 2 wk. Mean, systolic, and diastolic arterial pressures and heart rate of conscious unrestrained rats were unaffected. KMD-3213 reduced neointima growth by ~30 and 46% at the two doses (P < 0.01). These data support the novel hypothesis that a direct alpha 1A-adrenoceptor-dependent trophic action of catecholamines is augmented by injury and may contribute significantly to hypertrophic vascular disease.

adrenergic receptor; smooth muscle cell

* J. C. Teeters and C. Erami contributed equally to this work.




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