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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Ishibashi T, Kawada T, Kato K, Hamaguchi M, Imai S

Department of Pharmacology, Niigata University School of Medicine, Japan.

Gen Pharmacol. 1995 May;26(3):543-52. doi: 10.1016/0306-3623(94)00217-b.

Possible contribution of K+ channel opening to the relaxation by glyceryl trinitrate (GTN) was examined using isolated rabbit aorta. 2. While glibenclamide and apamin failed to affect relaxation by GTN, both charybdotoxin (ChTx) and iberiotoxin (IbTx) effectively attenuated GTN-induced relaxation. 3. The increase in cGMP produced by GTN was not attenuated by ChTx and IbTx. 4. The inhibitory effect of ChTx on GTN-induced relaxation was not reduced in the presence of zaprinast, indicating that cGMP but not GMP was responsible for activation of the K+ channel. 5. Okadaic acid, a selective inhibitor of protein phosphatase 2A, had no effect on the relaxation by GTN. These results indicate that, though small in degree, activation of a ChTx-sensitive K+ channel (large conductance Ca(2+)-activated K+ channel) is involved in the GTN-induced relaxation in rabbit aorta.

使用离体兔主动脉研究了钾通道开放对硝酸甘油（GTN）所致舒张作用的可能贡献。2. 格列本脲和蜂毒明肽未能影响GTN引起的舒张，但大蝎毒素（ChTx）和iberiotoxin（IbTx）均有效减弱了GTN诱导的舒张。3. GTN产生的cGMP增加未被ChTx和IbTx减弱。4. 在扎普司特存在的情况下，ChTx对GTN诱导舒张的抑制作用未降低，表明是cGMP而非GMP负责钾通道的激活。5. 冈田酸是蛋白磷酸酶2A的选择性抑制剂，对GTN引起的舒张无影响。这些结果表明，尽管程度较小，但ChTx敏感的钾通道（大电导钙激活钾通道）的激活参与了兔主动脉中GTN诱导的舒张。

Ishibashi T, Kawada T, Kato K, Hamaguchi M, Imai S

Department of Pharmacology, Niigata University School of Medicine, Japan.

Gen Pharmacol. 1995 May;26(3):543-52. doi: 10.1016/0306-3623(94)00217-b.

Possible contribution of K+ channel opening to the relaxation by glyceryl trinitrate (GTN) was examined using isolated rabbit aorta. 2. While glibenclamide and apamin failed to affect relaxation by GTN, both charybdotoxin (ChTx) and iberiotoxin (IbTx) effectively attenuated GTN-induced relaxation. 3. The increase in cGMP produced by GTN was not attenuated by ChTx and IbTx. 4. The inhibitory effect of ChTx on GTN-induced relaxation was not reduced in the presence of zaprinast, indicating that cGMP but not GMP was responsible for activation of the K+ channel. 5. Okadaic acid, a selective inhibitor of protein phosphatase 2A, had no effect on the relaxation by GTN. These results indicate that, though small in degree, activation of a ChTx-sensitive K+ channel (large conductance Ca(2+)-activated K+ channel) is involved in the GTN-induced relaxation in rabbit aorta.

使用离体兔主动脉研究了钾通道开放对硝酸甘油（GTN）所致舒张作用的可能贡献。2. 格列本脲和蜂毒明肽未能影响GTN引起的舒张，但大蝎毒素（ChTx）和iberiotoxin（IbTx）均有效减弱了GTN诱导的舒张。3. GTN产生的cGMP增加未被ChTx和IbTx减弱。4. 在扎普司特存在的情况下，ChTx对GTN诱导舒张的抑制作用未降低，表明是cGMP而非GMP负责钾通道的激活。5. 冈田酸是蛋白磷酸酶2A的选择性抑制剂，对GTN引起的舒张无影响。这些结果表明，尽管程度较小，但ChTx敏感的钾通道（大电导钙激活钾通道）的激活参与了兔主动脉中GTN诱导的舒张。