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.
Griffith
Tudor M
TM
Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff, UK. Griffith@cardiff.ac.uk
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