Since the discovery of endothelium-derived hyperpolarizing factor (EDHF), several different candidates and pathways have been proposed as mediators of endothelium-dependent hyperpolarization of vascular smooth muscle. In particular, there has been considerable support for a role for the cytochrome P450 metabolites, the epoxyeicosatrienoic acids (EETs). However, more recently, this hypothesis has come under severe scrutiny. In this issue of Clinical Science, Passauer et al. demonstrate that an EET cannot be EDHF in the human forearm, and add further to the growing belief that an EET is not a candidate for a ubiquitous EDHF.

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