Endothelium-dependent hyperpolarizing factor (EDHF) underlies nitric oxide and prostacyclin-independent arterial relaxation. As the influence of EDHF increases with decreasing artery size, it plays an important role in vascular regulation. Initially suggested to represent a diffusible factor, EDHF is now thought to represent a variable input in different arteries from a factor(s) and the spread of hyperpolarizing current from the endothelium to the smooth muscle. Key to unravelling this pathway has been the demonstration that hyperpolarization within the endothelium can be blocked using a combination of the <$E roman K sub Ca> channel blockers, apamin and charybdotoxin. As a consequence, the relaxation of vascular smooth muscle, which represents the end point of the EDHF pathway, is blocked. This review discusses the evidence that a differential distribution of ion channels between the smooth muscle and endothelial cells underlies the EDHF pathway. Also, that a diffusible factor, which may well be K ions released by the endothelium, acts alongside the spread of hyperpolarization through myoendothelial gap junctions to explain EDHF-evoked smooth muscle relaxation. While the relative importance of each of these two components can vary between arteries, together they can explain the EDHF phenomenon.

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