repaglinide Search Results


91
Toronto Research Chemicals 2 despiperidyl 2
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91
Tocris repaglinide
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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88
Toronto Research Chemicals repaglinide ethyl d5
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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85
Toronto Research Chemicals repaglinide d5
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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93
Tocris pnu 37883a
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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86
Toronto Research Chemicals 3 hydroxy repaglinide m4
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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90
Biosynth Carbosynth repaglinide
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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90
LKT Laboratories repaglinide rpg
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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90
Selleck Chemicals repaglinide
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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90
Santa Cruz Biotechnology repaglinide
( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker <t>repaglinide</t> (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.
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Image Search Results


( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker repaglinide (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.

Journal: Scientific Reports

Article Title: Inosine attenuates spontaneous activity in the rat neurogenic bladder through an A 2B pathway

doi: 10.1038/srep44416

Figure Lengend Snippet: ( A , B ) The attenuation of SA by inosine was reversed by the large conductance Ca 2+ -activated potassium channel blocker iberiotoxin (IBTX, 100 nM, n = 7). The SK3 channel blocker apamin (100 nM, n = 7) and the K ATP channel blocker repaglinide (10 μM, n = 8) did not prevent the attenuation of SA induced by inosine (**p < 0.01, **p < 0.001, Baseline versus Ino; *p < 0.05, Apamin versus Apamin + Ino, Regap versus Repag + Ino). ( C ) The attenuation of SA by the A 2B agonist BAY60-6583 (100 μM) was blocked by IBTX (100 nM, n = 5). Data are expressed as mean ± SEM, but with values normalised to drug alone, as opposed to baseline, as described in Methods.

Article Snippet: Reagents were purchased from suppliers as indicated: Inosine (Sigma-Aldrich, St. Louis, MO); CGS15943, MRS3777, PSB36, PSB603, ZM241385, PSB0777, NECA, BAY60-6583, repaglinide, iberiotoxin and apamin (Tocris Bioscience, Minneapolis, MN).

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