Original ArticleGynura procumbens Causes Vasodilation by Inhibiting Angiotensin II and Enhancing Bradykinin ActionsPoh, Ting-Fung; Ng, Hien-Kun; Hoe, See-Ziau PhD; Lam, Sau-Kuen PhDAuthor Information Department of Physiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. Reprints: Sau-Kuen Lam, PhD, Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia (e-mail: email@example.com). The experiments described in this report were funded by University of Malaya Research Grant (RG028-09BIO) and Postgraduate Research Grant (PS207-2010B) from the University of Malaya. The authors T. F. Poh and H. K. Ng were supported by University of Malaya Fellowship Scheme. The authors have no conflict of interest to declare. Received July 19, 2012 Accepted January 07, 2013 Journal of Cardiovascular Pharmacology: May 2013 - Volume 61 - Issue 5 - p 378-384 doi: 10.1097/FJC.0b013e31828685b3 Buy Metrics Abstract 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 Nω-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. © 2013 Lippincott Williams & Wilkins, Inc.