Endothelial-Derived Hyperpolarizing Factor (EDHF): Is there more than one?
It is now well established that the pharmacological properties of EDRF reflect those of nitric oxide (NO). Furthermore, in some blood vessels, prostacyclin (PGI2) also contributes to endothelium-dependent vasorelaxation. However, there is now increasing evidence, particularly from resistance vessels, that a factor(s), other than NO or PGI2, may play an important role in mediating endothelium-dependent hyperpolarization of vascular smooth muscle (Mombouli & Vanhoutte, 1997; Waldron et al. 1996). Recent studies from our laboratory indicate that in a large conduit vessel, the rabbit carotid artery, EDHF possesses the properties of a cytochrome P450 arachidonic acid product (Dong et al. 1997), whereas in mesenteric vessels from both the guinea pig and the rat, cytochrome P450 inhibitors have minimal effects on non-NO/PGI2 endothelium-dependent vasorelaxation. These data strongly suggest that EDHF is not a single entity and that tissue and species differences may exist.