Blockade of both α1A- and α1B-adrenergic receptor subtype signaling is required to inhibit neointimal formation in the mouse femoral artery

Abstract

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 α1-adrenergic receptors (α1-ARs) may facilitate restenosis after PCI because of α1-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 α1A-knockout (α1A-KO), α1B-KO, α1D-KO, α1A-/α1B-AR double-KO (α1AB-KO), and wild-type mice to investigate the functional role of each α1-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 α1AB-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 α1A- and α1B-ARs could be necessary to inhibit neointimal formation in the mouse femoral artery.