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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
3                                         When sarafotoxin 6b, which possesses modest matrix metallopro
4 using ETB-selective agonists ET-3, IRL-1620, sarafotoxin 6c (S6c) as well as ETA-selective antagonist
5  PD142893 (an ET(A/B) mixed antagonist), and sarafotoxin 6C (S6C; an ET(B) agonist).
6                   The ET(B) receptor agonist sarafotoxin 6c also reduced transport.
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
9                       ET(B) receptor agonist sarafotoxin also elicited concentration-dependent constr
10                                   Similarly, sarafotoxin, an ET-B-receptor agonist, was infused at th
11 with an enhanced vasoconstrictor response to sarafotoxin and suggests an alteration in coronary ET re
12                                          The sarafotoxins and endothelins are approximately 25-residu
13                 Previous work indicates that sarafotoxins and endothelins can be engineered to elimin
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
18             Before estradiol administration, sarafotoxin induced no net change in CSA but induced inc
19 tive ET(B) receptor-induced stimulation with sarafotoxin remained unchanged.
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
23         In cultured stellate cells, ET-1 and sarafotoxin S6C (a potent ETB receptor agonist) stimulat
24                               The effects of sarafotoxin S6C (a potent stellate cell contractile agon
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
27                                              Sarafotoxin S6c failed to induce any direct constriction
28                             Endothelin-1 and sarafotoxin S6C induced contractility of stellate cells
29                                     However, sarafotoxin S6c induced transient vasodilation at the in
30           Moreover, the inhibitory effect of sarafotoxin S6c on CFVs was completely abolished in the
31                              Both BQ-123 and sarafotoxin S6c significantly reduced CFVs represented b
32                                              Sarafotoxin S6C, an endothelin B (ETB) receptor agonist,
33 e because at ETB receptor-selective agonist, sarafotoxin S6c, was ineffective.
34 e mean luminal stenosis (BQ-123=29+/-13% and sarafotoxin S6c=27+/-11% reduction, respectively; P<.05
35                   An ET(B) receptor agonist, sarafotoxin (S6c, 30 ng. kg(-1). min(-1)) was administer
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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