Endothelial control of vascular tone by nitric oxide and gap junctions: a haemodynamic perspective.
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.
Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff, UK. Griffith@cardiff.ac.uk
Tudor M
TM
Griffith
D000818:Animals; D001161:Arteriosclerosis / Q000503:physiopathology; D001685:Biological Factors / Q000378:metabolism; D004730:Endothelium, Vascular / Q000502:physiology* / Q000503:physiopathology; D017629:Gap Junctions / Q000502:physiology*; D006439:Hemodynamics; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000502:physiology / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism*; D012039:Regional Blood Flow; D015398:Signal Transduction / Q000502:physiology*; D013314:Stress, Mechanical
D001685:Biological Factors; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide