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Editorial

Endothelium-Dependent Hyperpolarization: No Longer an F-Word!

Félétou, Michel PhD*; Vanhoutte, Paul M. MD, PhD

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Journal of Cardiovascular Pharmacology: February 2013 - Volume 61 - Issue 2 - p 91-92
doi: 10.1097/FJC.0b013e31828197bc
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From June 27 to June 29, 2012, a meeting was gathered in the mythical “Abbaye des Vaulx-de-Cernay,” in the middle of the sumptuous forest of Rambouillet, to discuss the latest knowledge on endothelium-dependent hyperpolarization (EDH) and related topics of endothelial function. This place is very dear to the lovers of endothelium-derived hyperpolarizing factors because it was host to a number of similar symposia in the late-90s and at the beginning of this millennium, which played a seminal role in disseminating knowledge in this then-bourgeoning area of vascular biology.

The reunion in 2012 celebrated the 10th anniversary of the last one held in the Abbey, and many of the initial movers and shakers in the field were present. Several of them, however, have left us forever, and the participants fondly remembered R. Furchgott, R. Busse, and T. Griffith, who passed away very recently, and was honored in the inaugural lecture, the First Tudor Griffith Memorial Lectured delivered masterfully by C. Hill. This year’s meeting concretized that diffusible factors1 cannot explain all EDHs and that cell-to-cell contacts and conduction play a prominent role, as perceived initially by Griffith et al.2 The identities of most diffusible endothelium-derived mediators that can cause EDH is now well established and should be referred to by their proper names (NO, CO, H2O2, H2S, and arachidonic acid derivatives)3,4 and when they are not involved cell-to-cell contacts explain the phenomenon. Thus, the term “endothelium-derived hyperpolarizing factor,”5 abbreviated to EDHF, should no longer be used because it masks the real identity of the signal(s) involved. In Vaulx-de-Cernay, we agreed that if an abbreviation is required, EDH should be preferred.

This supplement in the Journal of Cardiovascular Pharmacology, after the text of the Tudor Griffith Memorial Lecture,6 groups the introductory lectures to the different scientific sessions of the symposium. First, there is an update on the pharmacology of potassium channels, key players in EDH-mediated responses,7 followed by a summary of the role of the new channel on the block, TRPV4.8 The important contribution of endothelial 15-lipoxygenase eicosanoids is highlighted by the master in the field.9 The roles of different signaling cascades and enzymes, including adenosine monophosphate–activated protein kinase, hemoxygenase, and bone morphogenic protein-4, in endothelial function/dysfunction are emphasized.10 The unexpected impact of intrauterine growth on endothelial function in later life is revealed.11 Then, this supplement brings us back from molecular biology to the best model of disease, humans, and discusses the intricacies of endothelium-dependent control in our species.12

At the end of the symposium, it was clear that although the EDH field has matured, we still have a way to go to fully understand the role of the phenomenon, particularly in the brain circulation. The Editors hope that the knowledge summarized in this supplement will help vascular biologists at large to do so.

REFERENCES

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2. Chaytor AY, Evans WH, Griffith TM. Central role of heterocellular gap junction communication in endothelium-dependent relaxations of rabbit arteries. J Physiol (Lond). 1998;508:561–573.
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12. Bellien J, Joannides R. Epoxyeicosatrienoic acid pathway in human health and diseases. J Cardiovasc Pharmacol. In press.
© 2013 Lippincott Williams & Wilkins, Inc.