Blocking potassium channels: a new principle for treating restenosis?

摘要

Vascular smooth muscle cells are important for the structural integrity of the tunica media, but they are also central to vascular remodelling in response to injury. Although they are highly differentiated cells with the ability to regulate vascular tone and synthesize extracellular matrix, smooth muscle cells are also very plastic cells. This enables them to switch from a contractile to an invasive, migrating, and proliferating phenotype in response to local injury. Ion channels in the plasmalemma of smooth muscle cells have been implicated in this active process. There is evidence of profound changes in the types of ion channels that are expressed or functionally important during vascular smooth muscle cell transition resulting in occlusive vascular pathologies. In the systemic circulation, vessel restenosis remains a major factor limiting the success of balloon angioplasty/stenting of coronary, carotid, and femoral arteries. A critical event seems to be replacement of the K_Ca1.1 (BK_Ca) with the intermediate-conductance Ca~(2+)-activated potassium channel K_Ca3.1 and the loss of Cav1.2 (the L-type voltage-dependent) calcium channels.