selective et b receptor antagonist  (Alomone Labs)

Journal: Molecular Pain

Article Title: Endothelin receptor type A is involved in the development of oxaliplatin-induced mechanical allodynia and cold allodynia acting through spinal and peripheral mechanisms in rats

doi: 10.1177/17448069211058004

Figure Lengend Snippet: Systemic administration of a dual ET A /ET B receptor antagonist prevented oxaliplatin-induced mechanical allodynia and cold allodynia: Mechanical allodynia (a, b) and cold allodynia (c) were examined using the von Frey test and the acetone test, respectively. Bosentan (50 mg/kg) was intraperitoneally administered for 8 consecutive days (A; from days −1 to 6) and for 2 consecutive days (b and c; days −1 and 0) before intraperitoneal oxaliplatin administration ( n = 6). (a) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, and 14 days after oxaliplatin administration. (b) The dose–response relationship of bosentan was examined at day 1 after oxaliplatin administration. (c) Cold allodynia was performed before and 2 h, 8 h and 24 h after oxaliplatin administration. * p < 0.05 and ** p < 0.01, compared with the vehicle group using the Mann–Whitney U -test (a, c). ** p < 0.01, compared with the vehicle group using the Steel test (b). Pre: before administration of bosentan.

Article Snippet: Oxaliplatin (Yakult Corporation, Tokyo, Japan) was diluted in 5% glucose solution (1 mg/mL) and intraperitoneally administered at a dose of 5 mg/kg at day 0. , Bosentan, a dual ET A /ET B receptor antagonist (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), atrasentan, a selective ET A receptor antagonist (Sigma-Aldrich, St Louis, MO, USA) and BQ-788, a selective ET B receptor antagonist (Alomone Labs, Jerusalem, Israel) were dissolved in 60% dimethylsulfoxide and 40% propylene glycol.

Techniques: MANN-WHITNEY

Journal: Molecular Pain

Article Title: Endothelin receptor type A is involved in the development of oxaliplatin-induced mechanical allodynia and cold allodynia acting through spinal and peripheral mechanisms in rats

doi: 10.1177/17448069211058004

Figure Lengend Snippet: Systemic administration of an ET A receptor antagonist, but not an ET B receptor antagonist, prevented oxaliplatin-induced mechanical allodynia and cold allodynia: Mechanical allodynia (a, b, d) and cold allodynia (c, e) were examined using the von Frey test and the acetone test, respectively. An ET A receptor antagonist, atrasentan (a–c), or an ET B receptor antagonist, BQ-788 (d, e), was intraperitoneally administered for 2 consecutive days (days −1 and 0) before intraperitoneal oxaliplatin administration (5 mg/kg) on day 0 ( n = 5–8). (a, d) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, 14 days, 21 days, and 28 days after oxaliplatin administration. (c, e) Cold allodynia was examined before atrasentan, BQ-788 and oxaliplatin administration and 2 h, 8 h, 24 h and 4 days after oxaliplatin administration. * p < 0.05 and ** p < 0.01, compared with the vehicle group using the Mann–Whitney U -test. (b) The dose–response relationship of atrasentan was examined at day 1 after oxaliplatin administration. * p < 0.05, compared with the vehicle group using the Steel test. Pre: before administration of atrasentan or BQ-788.

Article Snippet: Oxaliplatin (Yakult Corporation, Tokyo, Japan) was diluted in 5% glucose solution (1 mg/mL) and intraperitoneally administered at a dose of 5 mg/kg at day 0. , Bosentan, a dual ET A /ET B receptor antagonist (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), atrasentan, a selective ET A receptor antagonist (Sigma-Aldrich, St Louis, MO, USA) and BQ-788, a selective ET B receptor antagonist (Alomone Labs, Jerusalem, Israel) were dissolved in 60% dimethylsulfoxide and 40% propylene glycol.

Techniques: MANN-WHITNEY

Journal: PLoS ONE

Article Title: Endothelin-Dependent Vasoconstriction in Human Uterine Artery: Application to Preeclampsia

doi: 10.1371/journal.pone.0016540

Figure Lengend Snippet: ( A ) Upper panel: Dose-response curves obtained by cumulative increases in the concentration of ET-1 (0.1 nM–0.1 µM) on basal tone (CTL,❍), after pre-incubation for 10 minutes with either an ET A receptor antagonist (BQ-123, 1 µM,•) or an ET B receptor antagonist (BQ-788, 1 µM,☐), or a mixture of both antagonists (BQ-123+788, 1 µM,▪). Lower panel: Average contraction of uterine artery induced by 10 nM ET-1 with or without a 10 minutes pre-incubation period with either BQ-123, BQ-788 or BQ123+788 each at 1 µM concentration. Data are expressed as a percentage of the contraction induced by Phe (10 µM). ( B ) Effects of ET receptor antagonists when arteries were contracted with ET-1 (0.1 µM). When maximal contraction was established, ET receptor antagonists were added at the same concentrations used in panel A as illustrated on typical recordings of variations of isometric tension (upper panels). Bar graph represents the average tension after the addition of the drugs, expressed as a percentage of the contraction induced by ET-1 (lower panel). In all experiments, values indicate the means ± S.E.M. of 10 different arteries with experiments performed in triplicate.

Article Snippet: The following compounds were used and all purchased from Sigma-Aldrich: human ET-1, sarafotoxin-S6c (selective ET B receptor agonist), BQ-123 (selective ET A receptor antagonist), BQ-788 (selective ET B receptor antagonist), nifedipine and nicardipine (DHP class of calcium channel blocker), hydralazine, labetalol (alpha/beta blocker) and alpha-methyldopa (á 2 -adrenergic agonist).

Techniques: Concentration Assay, Incubation

Journal: PLoS ONE

Article Title: Endothelin-Dependent Vasoconstriction in Human Uterine Artery: Application to Preeclampsia

doi: 10.1371/journal.pone.0016540

Figure Lengend Snippet: The effect of sarafotoxin S6c (1 µM) was analyzed with or without a 10-minute pre-incubation period with either 1 µM BQ-123, BQ-788, nifedipine or 10 mM EGTA, and compared to the contraction induced by ET-1 alone (0.1 µM). ( A ) Representative recordings of isometric tension changes illustrating the effect of sarafotoxin S6c in presence (right panel) or in absence (left panel) of BQ-123 (other drugs not shown). ( B ) Average contraction obtained with sarafotoxin S6c under basal conditions (CTL) or in the presence of BQ-123, BQ-788, EGTA or nifedipine. Data, expressed as a percentage of the contraction induced by ET-1 (0.1 µM) in the same experiment, indicate the means ± S.E.M. of 10 different arteries, with experiments performed in triplicate. *** p<0.0001.

Article Snippet: The following compounds were used and all purchased from Sigma-Aldrich: human ET-1, sarafotoxin-S6c (selective ET B receptor agonist), BQ-123 (selective ET A receptor antagonist), BQ-788 (selective ET B receptor antagonist), nifedipine and nicardipine (DHP class of calcium channel blocker), hydralazine, labetalol (alpha/beta blocker) and alpha-methyldopa (á 2 -adrenergic agonist).

Techniques: Incubation