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1 s that received an intracoronary infusion of sarafotoxin.
2 mol/L), the selective ET(B) receptor agonist sarafotoxin (1 pmol/L to 10 nmol/L), and serotonin (0.1
4 using ETB-selective agonists ET-3, IRL-1620, sarafotoxin 6c (S6c) as well as ETA-selective antagonist
7 nctional studies showed that ET-1, ET-3, and sarafotoxin 6c displayed similar potencies for inositol
8 eptor antagonist blocked effects of ET-1 and sarafotoxin 6c; an ET(A) receptor antagonist was without
11 with an enhanced vasoconstrictor response to sarafotoxin and suggests an alteration in coronary ET re
14 , support the hypothesis that the engineered sarafotoxins bind to matrix metalloproteinases in a mann
15 tagonist BQ788 abolished vasoconstriction to sarafotoxin but only slightly reduced responses to ET-1
16 on structure indicates a close similarity to sarafotoxin but with a more extended C-terminal helix.
17 ontrast, the administration of intracoronary sarafotoxin in TIVCC compared with normal dogs resulted
20 id (an inducer of differentiation), 10(-6) M sarafotoxin (S-6-c) (a selective ETB agonist), had a sim
21 tions of the selective endothelin-B agonist, sarafotoxin S6c (10(-11) to 10(-6) M), was measured in r
22 tivation was tested by the administration of sarafotoxin S6c (10(-7) to 10(-6) M) to rings preconstri
25 ects, P < .001), whereas vasoconstriction to sarafotoxin S6c (an ETB receptor agonist) was significan
26 (ETB receptor antagonist, 10 microg/min), or sarafotoxin S6c (ETB receptor agonist, 10 ng/min) was in
34 e mean luminal stenosis (BQ-123=29+/-13% and sarafotoxin S6c=27+/-11% reduction, respectively; P<.05
36 , which is an ETA receptor agonist, ET-3 and Sarafotoxin-S6c, two ETB receptor agonists, had little e
37 ences of peptides selected from libraries of sarafotoxin variants or suggested by analogy with tissue
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