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1 ffects of bosentan, an orally active ETA and ETB receptor antagonist.
2 1-fold control) and were inhibitable with an ET(B) receptor antagonist.
3 vel series of highly specific, orally active ET(B) receptor antagonists.
4 d proteins were blocked by an ET(A) (but not ET(B)) receptor antagonist.
5 (3 and 10 nmol/min); and BQ-788, a selective ET(B) receptor antagonist (0.3 and 1 nmol/min) using ven
6 receptor antagonist, 10 microg/min), BQ-788 (ETB receptor antagonist, 10 microg/min), or sarafotoxin
7 ist atrasentan (5 mg x kg(-1) x day(-1)), or ET(B) receptor antagonist A-192621 (15 mg x kg(-1) x day
10 Finally, the mixed endothelin-A (ETA) and ETB receptor antagonist, bosentan, reduced portal pressu
13 23 alone, and BQ-123 in combination with the ETB receptor antagonist BQ-788 after pretreatment with t
14 gated by pretreatment with the endothelin B (ET(B)) receptor antagonist, BQ-788, but not by the endot
16 ET(A) receptor antagonist BQ610, but not by ET(B) receptor antagonist BQ788, demonstrating that CNS-
17 In contrast, preincubation with a selective ETB receptor antagonist, BQ788 (1 mumol/L) significantly
19 s been shown that highly potent combined ETA/ETB receptor antagonists can be developed from the C-ter
21 eceptors for 28 days with only a mixed ET(A)/ET(B) receptor antagonist is insufficient to substantial
22 Intravenous pretreatment with another ET(A)/ET(B) receptor antagonist, L-754,142 (15 mg/kg as a bolu
23 ed by pretreatment with the endothelin ET(A)/ET(B) receptor antagonist, PD 145065 (48 micro g/2 micro
24 which were not inhibited by either ET(A) or ET(B) receptor antagonists, respectively BQ-123 and BQ78
26 ficacy of SB 217242, a nonpeptide dual ET(A)/ET(B) receptor antagonist with high oral bioavailability
27 gest that bosentan, an oral endothelin ET(A)/ET(B) receptor antagonist, with or without concomitant p
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