© 1999 American Heart Association, Inc.
Editorial |
Endothelium-Derived Hyperpolarizing Factors and Vascular Cytochrome P450 Metabolites of Arachidonic Acid in the Regulation of Tone
From the Departments of Pharmacology and Toxicology and Physiology and the Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wis.
Correspondence to William B. Campbell, PhD, Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail wbcamp@mcw.edu
Key Words: epoxyeicosatrienoic acid • 20-hydroxyeicosatetraenoic acid • K+ channel
The discovery of prostacyclin and its endothelial origin established the idea of endothelium-derived vasoactive eicosanoids and led to the realization that endothelial cells were a source of autacoids that regulate vascular tone.1 2 In 1980, Furchgott and Zawadzki3 described endothelium-derived relaxing factor (EDRF) and presented evidence that EDRF was a lipoxygenase metabolite of arachidonic acid. Subsequent research indicated that EDRF was nitric oxide.4 Several laboratories have described an endothelium-derived vasodilating factor that is distinct from nitric oxide or prostacyclin.5 6 7 8 9 10 These laboratories reported that acetylcholine caused endothelium-dependent relaxation and hyperpolarization of vascular smooth muscle. The relaxations and hyperpolarizations were not altered by arginine analogs that inhibit nitric oxide synthase or inhibitors of cyclooxygenase or lipoxygenases. They were blocked by inhibitors of calcium-activated potassium channels such as tetraethylammonium or charybdotoxin but not by inhibitors of ATP-sensitive potassium channels such as glibenclamide. Subsequent studies indicated that this factor was released by other agonists including bradykinin and substance P. It was concluded that this vasodilating factor acts by opening calcium-activated potassium channels and hyperpolarizing the smooth muscle membrane. This factor has been termed endothelium-derived hyperpolarizing factor or EDHF.
The article by Thollon and coworkers11 in this issue of
Circulation Research further emphasizes the importance of
EDHF in normal coronary arteries and arteries with regenerated
endothelium. Several important insights are provided
into the action and nature of EDHF by this work. First, this study
demonstrates the importance of measuring membrane potential in defining
the contribution of EDHF to the action of agonists.
Hyperpolarization of vascular smooth
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