α1-Adrenergic receptors mediate combined signals initiated by mechanical stretch stress and norepinephrine leading to accelerated mouse vein graft atherosclerosis

Our results demonstrated that α1-adrenergic receptors may partially mediate the intracellular signals induced by mechanical stretch with or without norepinephrine via Gαq protein/extracellular signal-regulated kinases pathway triggering increased proliferation of vascular smooth muscle cells and leading to accelerated neointima formation of vein grafts. These findings might advance current understanding of the potential effects of the coaction of hypertension mechanical stretch stress and increased norepinephrine in circulation due to sympathetic overdrive on vascular pathophysiology, and indicate a new role for α1-adrenergic receptors and related inhibitors in the pathogenesis and treatment of vascular remodeling.