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菊三七通过抑制血管紧张素 II 和增强缓激肽作用来引起血管舒张。

Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions.

机构信息

Department of Physiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.

出版信息

J Cardiovasc Pharmacol. 2013 May;61(5):378-84. doi: 10.1097/FJC.0b013e31828685b3.

Abstract

Previous studies showed that Gynura procumbens reduced blood pressure by blocking calcium channels and inhibiting the angiotensin-converting enzyme activity. The present experiments were to further explore the effects and mechanisms of a purer aqueous fraction (FA-I) of G. procumbens on angiotensin I (Ang I)-induced and angiotensin II (Ang II)-induced contraction of aortic rings and also on the bradykinin (BK) effect on cardiovascular system. Rat aortic rings suspended in organ chambers were used to investigate the vascular reactivity of FA-I. Effect of FA-I on BK was studied by in vitro and in vivo methods. Results show that FA-I significantly (P < 0.05) decreased the contraction evoked by Ang I and Ang II. In the presence of indomethacin (10 µM) or N-nitro-L-arginine methyl ester (0.1 µM), the inhibitory effect of FA-I on Ang II-induced contraction of aortic rings was reduced. Besides, FA-I potentiated the vasorelaxant effect and enhanced the blood pressure-lowering effect of BK. In conclusion, FA-I reduced the contraction evoked by Ang II probably via the endothelium-dependent pathways, which involve activation of the release of nitric oxide and prostaglandins. The inhibition of angiotensin-converting enzyme activity by FA-I may contribute to the potentiation of the effects of BK on cardiovascular system.

摘要

先前的研究表明,菊三七通过阻断钙通道和抑制血管紧张素转化酶的活性来降低血压。本实验进一步探讨了菊三七更纯的水提物(FA-I)对血管紧张素 I(Ang I)诱导和血管紧张素 II(Ang II)诱导的主动脉环收缩以及缓激肽(BK)对心血管系统作用的影响和机制。使用器官室中悬挂的大鼠主动脉环来研究 FA-I 的血管反应性。通过体外和体内方法研究 FA-I 对 BK 的作用。结果表明,FA-I 可显著(P<0.05)降低 Ang I 和 Ang II 引起的收缩。在吲哚美辛(10 µM)或 N-硝基-L-精氨酸甲酯(0.1 µM)存在的情况下,FA-I 对 Ang II 诱导的主动脉环收缩的抑制作用降低。此外,FA-I 增强了 BK 的血管舒张作用,并增强了其降低血压的作用。综上所述,FA-I 可能通过涉及一氧化氮和前列腺素释放的内皮依赖性途径来降低 Ang II 引起的收缩。FA-I 对血管紧张素转化酶活性的抑制可能有助于增强 BK 对心血管系统的作用。

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