SELE and hypertensive disorder: This could be through a direct release of vasoactive mediators or via endothelial KATP-mediated changes in endothelial cell membrane potential that is directly conducted to the smooth cells through myoendothelial gap junctions to produce vasorelaxation.18–23 However, the channel may more generally protect the endothelium against endothelial dysfunction such as would occur with the development of hypertension.31,32 In support, eKO mice also have elevated plasma E-selectin levels and diminished acetylcholine relaxation responses in mesenteric arteries.