硫前体L-氨酸和甘三酸盐之间的相互作用机制
Circulation
|September 1, 1992
概括
虽然L-氨酸增强了甘三酸盐 (GTN) 的作用,但其转化产物L-氨酸 (L-cysteine) 独立调节酸盐耐受性. 甲氨酸不能替代无酸盐的时间间隔,以恢复大容器的敏感性.
科学领域:
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
- 心血管生理学心血管生理学
背景情况:
- 甲氨酸增强了甘三酸盐 (GTN) 的作用,类似于N-乙半氨酸 (NAC).
- 这种增强与增强的尼特罗斯醇形成有关,刺激可溶性瓜尼利环酶.
- 这项研究调查了L-甲氨酸对GTN诱导的血管扩张和酸盐耐受性的直接影响.
研究的目的:
- 直接分析L-氨酸对GTN诱导的大脑大动脉扩张和狗的静脉容量的影响.
- 为了研究L-氨酸和GTN相互作用的细胞内和细胞外机制.
- 为了确定L-氨酸能否在耐受状态下恢复酸盐敏感性.
主要方法:
- 在清醒和麻醉的狗身上进行的实验 (不耐受和耐受状态).
- 测量包括血液动力学反应 (心跳动,低血压) 和心上动脉扩张.
- 在体外研究中使用了培养的老鼠大动脉光滑肌细胞和纯化瓜尼环酶.
主要成果:
- 在不耐受犬群中,L-甲氨酸增强了GTN的心率和低血压效应.
- 甲氨酸并没有改变GTN诱导的大脑大动脉扩张,也没有影响低压系统中的酸盐耐受性.
- 在体外,L-氨酸 (甲氨酸代谢物) 增强了GTN刺激的甘酸环酶活性,但L-甲氨酸没有增加细胞内硫含量.
结论:
- 作为L-氨酸的代谢物L-氨酸,可以独立于GTN强化,调解酸盐耐受性.
- 这种L-氨酸效应发生在抵抗血管中,而不是在大动脉或静脉中.
- 给予L-氨酸并不是治疗性替代无酸盐间隔,以恢复大型血管中的酸盐敏感性.
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