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(Hypertension. 2006;48:211.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Clarifying Endothelin Type B Receptor Function

David M. Pollock; Markus P. Schneider

From the Vascular Biology Center, Medical College of Georgia, Augusta.

Correspondence to David M. Pollock, Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912-2500. E-mail dpollock@mcg.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Endothelin (ET) receptors have become the targets for the treatment of a variety of cardiovascular disorders and a mixed ET type A (ET_A)/ET type B (ET_B) receptor antagonist, bosentan, is currently being used to effectively treat pulmonary hypertension. An ongoing debate has revolved around the question of whether selective ET_A receptor blockade would be preferable to using the mixed antagonist. The functional role of ET-1 is complicated by the opposing actions of the ET_A and ET_B receptor in the vasculature, as well as the kidney. ET_B receptor function is further complicated by the presence of vasoconstrictor ET_B receptors on vascular smooth muscle in some vascular beds, whereas ET_B receptors on endothelium and renal tubules have vasodilator and natriuretic activities. ET_B receptors also serve to clear ET-1 from the circulation and, thus, minimize vasoconstrictor activity. Despite the well-recognized effects of ET_B receptors to oppose ET_A-mediated actions, it is not clear whether blocking both ET_A and ET_B receptors at the same time is detrimental or advantageous compared with selective ET_A blockade. Indeed, ET_A selective antagonists are also expected to soon receive approval for treatment of pulmonary hypertension. Although this may indicate that both strategies work in pulmonary hypertension, the pros and cons of selective versus mixed antagonists are much less clear in arterial hypertension and heart and kidney failure.

Previous studies have shown that pharmacological blockade or genetic deficiency of ET_B receptors results in salt-sensitive hypertension in rats.^1,2 More recent studies have now provided information on the location(s) of . . . [Full Text of this Article]

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