Increased immunoreactivity of endothelin-1 and endothelin B receptor in human atherosclerotic lesions. A possible role in atherogenesis

Minimally modified LDL upregulates endothelin type B receptors in rat coronary artery via ERK1/2 MAPK and NF-κB pathways

“…There are two types of endothelin receptors in the vessel, endothelin type A (ET A ) and endothelin type B (ET B ). The ET receptors on the vascular smooth muscle cells are involved in the atherosclerotic process by enhancing contraction and proliferation of the smooth muscle cells [5][6][7]. The ET B receptors exhibit plasticity to adapt to the environmental changes.…”

“…The ET B receptors exhibit plasticity to adapt to the environmental changes. The upregulation of ET-1 and its receptors plays an important role in the pathogenesis of coronary vascular diseases and in the formation of atherosclerotic lesions in animals [8,9] and in man [7,10]. The ET B receptor is the principal receptor involved in the progression of coronary vascular diseases [5,7].…”

MEK1/2 inhibition attenuates vascular ETA and ETB receptor alterations after cerebral ischaemia

“…The endothelin system has been shown to be involved in several pathophysiological conditions, such as atherosclerosis (Iwasa et al 1999), heart failure (Miyauchi and Goto 1999) and ischaemic stroke (Ziv et al 1992;Barone et al 1994;Lampl et al 1997). After middle cerebral artery occlusion (MCAO) in cat, there is an enhanced ET mediated constriction in ischaemic vessels (Patel et al 1996b).…”

Endothelial dysfunction in atherosclerotic mice: improved relaxation by combined supplementation with L‐arginine‐tetrahydrobiopterin and enhanced vasoconstriction by endothelin

“…ET-1 has been proposed to be involved in the pathogenesis of several cardiovascular disorders including atherosclerosis (Kowala, 1997). The expression of ET converting enzyme, ET-1 and the ET B receptor subtype is enhanced in human atherosclerotic plaques (Kowala, 1997;Iwasa et al, 1999). Experimental studies have demonstrated that the constrictor response to exogenous ET-1 is more pronounced in large arteries of atherosclerotic monkeys than in control animals (Kowala, 1997).…”