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Am J Physiol Heart Circ Physiol (September 19, 2002). doi:10.1152/ajpheart.00658.2002
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Articles in PresS, published online ahead of print September 19, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00658.2002
Submitted on July 25, 2002
Accepted on September 9, 2002

Systemic [alpha]1A-adrenoceptor Antagonist Inhibits Neointimal Growth After Balloon Injury of Rat Carotid Artery

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

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

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 µg/kg and 32 µg/kg KMD-3213 had no effect on arterial pressure or renal and hindquarters resistances in anesthetized rats. A second group then received carotid balloon injury and continuous intravenous KMD-3213 at 4 and 10 µg/kg/h for two weeks. Mean, systolic and diastolic arterial pressures and heart rate of conscious unrestrained rats were unaffected. KMD-3213 reduced neointima growth by approximately 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.




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