1. Angiotensin II (AII) elicited only a minute, if any, direct contractile response in smooth muscle cells of prostatic rat vas deferens, but it potentiated contractile responses to field stimulation. 2. Angiotensin-potentiated contractile response to field stimulation was concentration-dependent, and the order of potency was AII > AIII approximately AI. The EC50 of AII was 8.11 +/- 2.79 nM. 3. AII did not modify the contractile response of exogenous noradrenaline (NA) on non-stimulated prostatic vas deferens. Furthermore, the concentration-response curve for AII-potentiated contractile responses to field stimulation in reserpine-treated rats did not significantly differ from the control group. 4. Desensitization of purinoceptors with 30 microM alpha, beta-methylene-ATP almost completely abolished the potentiation of the contractile response to field stimulation by AII. 5. The response to AII in the prostatic rat vas deferens was blocked by the AT1 selective antagonist losartan, but not by the AT2 selective antagonist CGP 42112. Losartan acted as a competitive antagonist with a pA2 value of 8.75. 6. In conclusion, AII potentiated purinergic transmission in the prostatic rat vas deferens via the AT1 receptor.

译文

1.血管紧张素II (AII) 仅在前列腺大鼠输精管的平滑肌细胞中引起一分钟 (如果有的话) 的直接收缩反应,但它增强了对场刺激的收缩反应。2.对场刺激的血管紧张素增强收缩反应是浓度依赖性的,效力顺序为AII> AII。AII的EC50为8.11 +/- 2.79纳米。3. AII没有改变外源性去甲肾上腺素 (NA) 对非刺激的前列腺输精管的收缩反应。此外,在利血平治疗的大鼠中,AII增强对场刺激的收缩反应的浓度-反应曲线与对照组没有显着差异。4.用30微m α,β-亚甲基-ATP对嘌呤受体的脱敏几乎完全消除了AII对场刺激的收缩反应的增强作用。5.前列腺大鼠输精管对AII的反应被AT1选择性拮抗剂氯沙坦阻断,但不是被AT2选择性拮抗剂CGP 42112阻断。氯沙坦作为竞争性拮抗剂,pA2值为8.75。6.总之,AII通过AT1受体增强了前列腺大鼠输精管中的嘌呤能传递。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录