The endothelin ETB receptor mediates both vasodilation and vasoconstriction in vivo

Evidence from receptor antagonists of an important role for ETB receptor‐mediated vasoconstrictor effects of endothelin‐1 in the rat kidney

“…In addition, we have also shown that BQ-123 was unable to block completely the pressor effects of ET/SX peptides in the anaesthetized, ganglion-blocked rat (McMurdo et al, 1993). This non-ETA-mediated vasoconstriction may be due to ETB receptor activation (Ihara et al, 1991;Fukuroda et al, 1992;Clozel et al, 1993) or to a yet to be characterised novel ET receptor (Pollock & Opgenorth, 1993;Warner et al, 1993).…”

In vitro characterisation of Ro 46‐8443, the first non‐peptide antagonist selective for the endothelin ETB receptor

“…It has been demonstrated that not only ETA but also ETB receptors can mediate vaso-or bronchoconstriction [4][5][6]. Furthermore, the importance of ETB receptors in pathological situations may be reflected by enhanced receptor densities as recently described for the aorta of spontaneously hypertensive rats [9], the basilar artery of rabbits after subarachnoidal hemorrhage [11] and for the rabbit carotid artery after balloon denudation [29].…”

Endothelium-Dependent Vasoconstriction in Isolated Vessel Grafts: A Novel Mechanism of Vasospasm?

“…In contrast, basal HSV tones in the present study were not affected by L-NAME, and these vessels responded only weakly to endothelium-dependent vasodilators (data not shown), demonstrating endothelial dysfunction. ET binding to ET-1B receptors on endothelial cells induces vasorelaxation in healthy vessels [32], although a constricting mechanism was demonstrated in rat vessels [33]. This constricting mechanism becomes dominant under pathological conditions, with ET-1 causing endothelium-dependent vasoconstrictions that involve the release of endothelium-derived contracting factors (EDCF) [34].…”