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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

Shinkai-Goromaru M, Samejima H, Takayanagi I

Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences, Chiba, Japan.

Gen Pharmacol. 1997 Mar;28(3):365-9. doi: 10.1016/s0306-3623(96)00291-1.

We determined the endothelin (ET) receptor subtype involved in the facilitation of electrical field stimulation-(EFS) induced contraction using the ETB receptor agonist sarafotoxin S6c (STX S6c) and the ET receptor antagonists TTA-386 and bosentan. 2. ET-3-and ETB-receptor-selective agonist STX S6c enhanced EFS-induced contractions. The increasing effect of ET-3 was partially reduced by the desensitization to STX S6c or the ETA receptor antagonist TTA-386. After simultaneous treatment with TTA and desensitization, ET-3-induced potentiation was completely abolished. The combined ETA/B receptor blocker bosentan (Ro 47-0203) eliminated the ET-3-evoked neuronal effect. Both ETB and ETA receptors are involved in the facilitating effects of ETs on EFS contraction. 3. ET-3 immunoreactivity occurs densely in this tissue and was released from neuronal sites by electrical stimulation. We suggest that endogenous ET-3 has a more predominant role than ET-1.

我们使用内皮素B（ETB）受体激动剂沙拉新（STX S6c）以及内皮素（ET）受体拮抗剂TTA - 386和波生坦，确定参与电场刺激（EFS）诱导收缩促进作用的ET受体亚型。2. ET - 3及ETB受体选择性激动剂STX S6c增强了EFS诱导的收缩。ET - 3的增强作用因对STX S6c脱敏或ETA受体拮抗剂TTA - 386而部分减弱。TTA与脱敏同时处理后，ET - 3诱导的增强作用完全消除。ETA/B受体联合阻滞剂波生坦（Ro 47 - 0203）消除了ET - 3诱发的神经元效应。ETB和ETA受体均参与ET对EFS收缩的促进作用。3. ET - 3免疫反应性在该组织中密集存在，并通过电刺激从神经元部位释放。我们认为内源性ET - 3比ET - 1发挥更主要的作用。

Shinkai-Goromaru M, Samejima H, Takayanagi I

Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences, Chiba, Japan.

Gen Pharmacol. 1997 Mar;28(3):365-9. doi: 10.1016/s0306-3623(96)00291-1.

We determined the endothelin (ET) receptor subtype involved in the facilitation of electrical field stimulation-(EFS) induced contraction using the ETB receptor agonist sarafotoxin S6c (STX S6c) and the ET receptor antagonists TTA-386 and bosentan. 2. ET-3-and ETB-receptor-selective agonist STX S6c enhanced EFS-induced contractions. The increasing effect of ET-3 was partially reduced by the desensitization to STX S6c or the ETA receptor antagonist TTA-386. After simultaneous treatment with TTA and desensitization, ET-3-induced potentiation was completely abolished. The combined ETA/B receptor blocker bosentan (Ro 47-0203) eliminated the ET-3-evoked neuronal effect. Both ETB and ETA receptors are involved in the facilitating effects of ETs on EFS contraction. 3. ET-3 immunoreactivity occurs densely in this tissue and was released from neuronal sites by electrical stimulation. We suggest that endogenous ET-3 has a more predominant role than ET-1.

我们使用内皮素B（ETB）受体激动剂沙拉新（STX S6c）以及内皮素（ET）受体拮抗剂TTA - 386和波生坦，确定参与电场刺激（EFS）诱导收缩促进作用的ET受体亚型。2. ET - 3及ETB受体选择性激动剂STX S6c增强了EFS诱导的收缩。ET - 3的增强作用因对STX S6c脱敏或ETA受体拮抗剂TTA - 386而部分减弱。TTA与脱敏同时处理后，ET - 3诱导的增强作用完全消除。ETA/B受体联合阻滞剂波生坦（Ro 47 - 0203）消除了ET - 3诱发的神经元效应。ETB和ETA受体均参与ET对EFS收缩的促进作用。3. ET - 3免疫反应性在该组织中密集存在，并通过电刺激从神经元部位释放。我们认为内源性ET - 3比ET - 1发挥更主要的作用。