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摘要: Endothelium-dependent hyperpolarizing factor or EDHF underlies nitric oxide and prostacylin independent arterial relaxation. As the influence of increases with decreasing artery size, it appears to play an important role in control blood pressure flow. Initially suggested represent a diffusible factor, is now recognised as pathway encompassing variable input different arteries from factor(s) spread current endothelium smooth muscle. Key unravelling this has been demonstration that hyperpolarization within can be blocked using combination toxins apamin charybdotoxin. consequence, relaxation vascular muscle, which represents end point EDHF-pathway, also blocked. This review discusses evidence operates vivo modified cardiovascular disease. Also discussed are mechanisms responsible for EDHF-evoked vasodilatation, focusing on localization specific potassium (K) channels endothelium, may well K ion released by endothelial cells, acts alongside through myoendothelial gap junctions evoke EDHF-linked While relative importance each these components vary arteries, together they explain phenomenon.