Shear stress and intermediate-conductance calcium-activated potassium channels

See article by Brakemeier et al. [4] (pages 488–496) in this issue. Vascular endothelial cells (EC) are continuously exposed to shear stress associated with the flowing blood. Over the years, it has become clear that such shear exerts a multitude of effects on endothelial biology and vascular function and structure, ranging in time span from seconds to months. On the scale of seconds, shear-dependent vasodilation has been demonstrated in many experimental settings. In the course of months, shear stress is believed to shape the vascular bed through remodeling [1]. Thus, shear stress sensing provides a mechanistic base for the notion of Murray in 1926 that vascular diameter should be proportional to the cube of the carried flow in order to minimize the costs of maintaining a circulation [2]. Steady laminar shear is atheroprotective while low shear levels and temporal or spatial variation of shear have been related to development of atherosclerosis [3]. Considering the clear importance of shear stress, much research is devoted to identifying the mechanisms of shear stress sensing, the intracellular processes that occur in response to altered shear stress patterns, and the functional and structural consequences. The paper by Brakemeier et al., in this issue [4], shows that expression of intermediate-conductance calcium-activated potassium channel in human umbilical vein endothelial cells (HUVECs) is upregulated by arterial shear stress. The authors suggest that such upregulation could form a mechanism for long-term adaptation of endothelial cells to altered blood flow [4].