Endothelial control of vascular tone by nitric oxide and gap junctions: A haemodynamic perspective

Abstract

Local haemodynamic forces acting on the endothelium modulate vascular tone through mechanisms that normalize intimal shear stress. This flow‐dependent diameter response contributes to the optimization of circulatory function and is mediated via shear stress‐induced release of NO, vasodilator prostanoids and a putative endothelium‐derived hyperpolarizing factor or EDHF. There is growing evidence that NO/prostanoid independent relaxations involve direct heterocellular signalling between endothelial and smooth muscle cells via gap junctions.