Endothelial dysfunction of conduit arteries contributes to the increased morbidity and
cardiovascular mortality in patients with essential hypertension and appears increasingly as
an independent therapeutic target. We have shown previously that besides a decrease in the
availability of NO and other endothelium-derived vasodilators factors, the
epoxyeicosatrienoic acids, an increase in the vasoconstrictor endothelin-1 (ET-1) may play a
role in the pathophysiology of this endothelial dysfunction. Indeed, the local concentrations
of endothelin-1 during the endothelium-dependent dilation of the radial artery in response to
a sustained increase in blood flow decreased significantly in healthy volunteers controls but
not in hypertensive patients. This lack of adaptation of the endothelinergic system could be
due to a decreased clearance of endothelin-1 by endothelial ETB receptors, potentiating the
vasoconstrictor action of endothelin-1 mediated by ETA receptor activation at the muscular
level. However, to validate this hypothesis , it is needed to demonstrate the physiological
role of ETA receptor and ETB in sustained flow-mediated dilatation of conduit arteries.