Tudor Griffith, gap junctions and conducted vasodilatation: electromechanical coupling back in the limelight.
Tudor Griffith's untimely death cut short a research career focused on the mechanisms regulating vascular tone and blood flow. This brief review highlights the contribution that Tudor's work made to 3 main areas: the early days of study toward elucidating the identity of the endothelium-derived relaxing factor (or nitric oxide), the use of computational modeling to unravel the mechanisms underlying the rhythmical arterial contractions known as vasomotion, and the role played by gap junctions in the vasodilatation attributed to endothelium-derived hyperpolarization. Tudor's pioneering application of the connexin mimetic peptides as selective gap junction antagonists has contributed substantially to the current state of knowledge on the role of cell coupling in arterial function. Together, these studies have reemphasized the importance of electromechanical coupling by which changes in membrane potential can rapidly control vessel diameter and blood flow.
Department of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, Australia. caryl.hill@anu.edu.au
Caryl E
CE
Hill
D000818:Animals; D001685:Biological Factors / Q000266:history / Q000378:metabolism*; D017630:Connexins / Q000378:metabolism; D017629:Gap Junctions / Q000378:metabolism*; D049673:History, 20th Century; D049674:History, 21st Century; D006801:Humans; D008564:Membrane Potentials / Q000502:physiology; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D012039:Regional Blood Flow / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*
D001685:Biological Factors; D017630:Connexins; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide