Endothelium-derived hyperpolarizing factor 3225221 213334059 2008-05-18T21:44:41Z CmdrObot 1079367 sp: phenomonenon→phenomenon '''Endothelium-derived hyperpolarizing factor''' or '''EDHF''' refers to an unknown compound, secreted by [[endothelium|endothelial cells]], which leads to [[nitric oxide]]- and [[prostacyclin]]-independent [[vasodilation]] by relaxation of [[Blood vessel|vascular]] [[smooth muscle|smooth muscle cells]]. ==Discovery of EDHF== Secretion of nitric oxide (NO) or prostacyclin by endothelial cells causes vascular smooth muscle cell relaxation. In experiments in which both NO and prostacyclin production are inhibited, [[arteriole|arterioles]] still continue to dilate if they are stimulated (e.g. by [[acetylcholine]] or [[bradykinin]]), causing [[vasodilation]] which causes blood flow to increase. This observed increase in [[blood vessel]] dilation is inhibited by [[potassium]] channels blockers; therefore this method of vessel dilation relies on an endothelium-dependent [[Hyperpolarization (biology)|hyperpolarization]] of the smooth muscle cells. This unknown factor(s) secreted by endothelial cells has been termed endothelium-derived hyperpolarizing factor. ==Mechanism== Endothelium-derived hyperpolarizing factor vasodilates by causing [[hyperpolarization]]<ref name=boron> {{cite book |author=Walter F., PhD. Boron |title=Medical Physiology: A Cellular And Molecular Approaoch |publisher=Elsevier/Saunders |location= |year=2005 |pages= |isbn=1-4160-2328-3 |oclc= |doi=}} Page 480 </ref>, hence the name. ==Chemical Identity== Although the phenomenon of EDHF has been observed and reported in scientific literature, to date the chemical identity of the factor(s) has not been determined. Although some researchers believe the EDHF is potassium ions, other researchers have shown evidence that an [[endocannabinoid]] ([[anandamide]]) might be involved by activating the [[CB1 receptor]]; although the role of anandamide in EDHF has been discounted, as its action has now been shown to occur via a non-endothelium-dependent mechanism. In some cases, members of a class of [[arachidonic acid]] derivatives, the [[epoxyeicosatrienoic acid|epoxyeicosatrienoic acids]] (EETs), have been found to mediate the vasodilation. These compounds are formed by [[epoxidation]] of any one of four [[double bonds]] of the arachidonic acid carbon backbone by [[cytochrome]] [[P450]] epoxygenase enzymes. In addition, in some cases [[hydrogen peroxide]] has been suggested to function as an EDHF in some vascular beds; although the validity of this observation is debated by several groups. [[Gap junction]]al coupling between the endothelium and smooth muscle, has also been implicated in EDHF activity in many arteries, whereby 'EDHF' activity may simply be due to the transfer of an EDH, and not to the activity of a Factor ''per se''. ==References== <references/> {{circulatory-stub}} [[Category:Biomolecules]] [[Category:Vasodilators]] [[Category:Cardiovascular system]] [[it:EDHF]]