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Endothelium-derived hyperpolarizing factor: a cousin to nitric oxide and prostacyclin Bryan RM Jr; You J; Golding EM; Marrelli SPAnesthesiology 2005[Jun]; 102 (6): 1261-77There is now strong evidence that an endothelial mechanism, other than nitric oxide or prostacyclin, exists for dilating arteries and arterioles. This third pathway has been named endothelium-derived hyperpolarizing factor (EDHF) and should not be confused with endothelium-derived relaxing factor, which is nitric oxide. Currently, there are several ideas for the mechanism of EDHF, which may vary among vessels of different organs and species. During some pathologic states, EDHF can be up-regulated. This up-regulation often occurs as the dilator effects of endothelium-derived nitric oxide are suppressed. The up-regulated EDHF may serve in a protective capacity to help maintain blood flow to organs and tissues during these stressful states. Many anesthetics attenuate the dilator actions of EDHF; however, the full clinical implications of this anesthetic-related attenuation are not known. Like its cousins, nitric oxide and prostacyclin, EDHF is an important regulator of blood flow and should prove to be an important clinical consideration as we gain more knowledge of its mechanisms of action.|Animals[MESH]|Biological Factors/chemistry/*physiology[MESH]|Endothelium, Vascular/chemistry/*physiology[MESH]|Epoprostenol/chemistry/*physiology[MESH]|Humans[MESH]|Muscle, Smooth, Vascular/chemistry/physiology[MESH]|Nitric Oxide/chemistry/*physiology[MESH] |
