Evidence against C‐type natriuretic peptide as an arterial ‘EDHF’

C-type natriuretic peptide (CNP) is found in and released from vascular endothelial cells. Recently, a novel role has been suggested for this peptide, that of an endothelium-derived hyperpolarizing factor or EDHF. Implicit in this proposal is a widespread role for CNP as a key mediator of vascular dilatation. In this issue of the British Journal of Pharmacology, Leuranguer et al. compare the profile of membrane potential changes evoked with this putative EDHF or with endogenous EDHF (activated with ACh) in small carotid arteries. Marked differences between the two profiles lead them to discount a possible role for CNP as an EDHF.