Endothelin-A Receptor Antagonist-Mediated Vasodilatation Is Attenuated by Inhibition of Nitric Oxide Synthesis and by Endothelin-B Receptor Blockade

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Abstract

Background

The role of endothelin (ET)-1 in maintenance of basal vascular tone has been demonstrated by local and systemic vasodilatation to endothelin receptor antagonists in humans. Although the constrictor effects mediated by the vascular smooth muscle ETA receptors are clear, the contribution from endothelial and vascular smooth muscle ET (B) receptors remains to be defined. The present study, in human forearm resistance vessels in vivo, was designed to further investigate the physiological function of ETA and ETB receptor subtypes in human blood vessels and determine the mechanism underlying the vasodilatation to the ETA -selective receptor antagonist BQ-123.

Conclusions

Selective ETA receptor antagonism causes vasodilatation of human forearm resistance vessels in vivo. This response appears to result in major part from an increase in nitric oxide generation. ETB receptor antagonism either alone or on a background of ETA antagonism causes local vasoconstriction, indicating that ETB receptors in blood vessels respond to ET-1 predominantly by causing vasodilatation. (Circulation. 1998;97:752-756.)

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