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Endothelin Receptor
ETs represent a group of three distinctive 21-amino acid peptides: ET-1, ET-2, and ET-3, with ET-1 being the main isoform produced in the cardiovascular system. Each ET isoform is synthesized as a large pre proendothelin(pre-pro-ET) that is cleaved to pro-ET (big ET-1, -2, and -3) and then further processed by ET-converting enzymes (ECE-1 and ECE-2) to yield mature ET. ET-1 exerts its action through two pharmacologically distinct G protein-coupled receptors, namely, ETA and ETB receptors. The ETA receptor is mostly expressed on vascular smooth muscle cells, fibroblasts, and cardiomyocytes and mediates the vasoconstrictor and proliferative effects of ETs. The ETB receptor is expressed on vascular endothelial cells where it induces endothelial-dependent vasodilatation through NO production and clearance of circulating ET-1.
The ETB receptor is also present on vascular smooth muscle cells, where its activation induces vasoconstriction and cell proliferation, and on fibroblasts, where it mediates cell proliferation, matrix contraction, and collagen production. Both ETA and ETB receptors mediate the detrimental actions of ET-1. Because of a “cross talk” between ETA and ETB receptors, selective antagonism of only one receptor subtype may result in compensation by the other receptor subtype and may be insufficient, whereas dual antagonism may be necessary for complete inhibition. The molecular basis of this cross talk between receptors could be the formation of ETA–ETB heterodimers in cells expressing both receptor subtypes, which may further modulate the functionality of the receptors.
The ETB receptor is also present on vascular smooth muscle cells, where its activation induces vasoconstriction and cell proliferation, and on fibroblasts, where it mediates cell proliferation, matrix contraction, and collagen production. Both ETA and ETB receptors mediate the detrimental actions of ET-1. Because of a “cross talk” between ETA and ETB receptors, selective antagonism of only one receptor subtype may result in compensation by the other receptor subtype and may be insufficient, whereas dual antagonism may be necessary for complete inhibition. The molecular basis of this cross talk between receptors could be the formation of ETA–ETB heterodimers in cells expressing both receptor subtypes, which may further modulate the functionality of the receptors.
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