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Am J Physiol Heart Circ Physiol 293: H514-H519, 2007. First published March 23, 2007; doi:10.1152/ajpheart.00626.2006
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Blockade of both {alpha}1A- and {alpha}1B-adrenergic receptor subtype signaling is required to inhibit neointimal formation in the mouse femoral artery

Chihiro Hosoda,1,2,* Masami Hiroyama,1,* Atsushi Sanbe,1 Jun-ichi Birumachi,1 Tadaichi Kitamura,2 Susanna Cotecchia,3 Paul C. Simpson,4 Gozoh Tsujimoto,5 and Akito Tanoue1

1Department of Pharmacology, National Research Institute for Child Health and Development, Tokyo, Japan; 2Department of Urology, Faculty of Medicine, University of Tokyo, Tokyo, Japan; 3Institut de Pharmacologie et Toxicologie, Universit de Lausanne, Lausanne, Switzerland; 4Cardiology Division, San Francisco Veterans Affairs Medical Center, and the Cardiovascular Research Institute and Department of Medicine, University of California San Francisco, San Francisco, California; and 5Department of Genomic Drug Discovery Science, Graduate School of Pharmaceutical Sciences, Kyoto University Faculty of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan

Submitted 13 June 2006 ; accepted in final form 22 March 2007

Attenuation of early restenosis after percutaneous coronary intervention (PCI) is important for the successful treatment of coronary artery disease. Some clinical studies have shown that hypertension is a risk factor for early restenosis after PCI. These findings suggest that {alpha}1-adrenergic receptors ({alpha}1-ARs) may facilitate restenosis after PCI because of {alpha}1-AR's remarkable contribution to the onset of hypertension. In this study, we examined the neointimal formation after vascular injury in the femoral artery of {alpha}1A-knockout ({alpha}1A-KO), {alpha}1B-KO, {alpha}1D-KO, {alpha}1A-/{alpha}1B-AR double-KO ({alpha}1AB-KO), and wild-type mice to investigate the functional role of each {alpha}1-AR subtype in neointimal formation, which is known to promote restenosis. Neointimal formation 4 wk after wire injury was significantly (P < 0.05) smaller in {alpha}1AB-KO mice than in any other group of mice, while blood pressures were not altered in any of the groups of mice after wire injury compared with those before it. These results suggest that lack of both {alpha}1A- and {alpha}1B-ARs could be necessary to inhibit neointimal formation in the mouse femoral artery.

{alpha}1-adrenergic receptor; vascular injury; smooth muscle cell; femoral artery of mouse; wire injury


Address for reprint requests and other correspondence: A. Tanoue, Dept. of Pharmacology, National Research Institute for Child Health and Development, 2-10-1, Okura, Setagaya-ku, Tokyo 157-8535, Japan (e-mail: atanoue{at}nch.go.jp)






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