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.
|Number of pages||2|
|Journal||Proceedings of the Western Pharmacology Society|
|Publication status||Published - 1998|
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