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

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...

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Main Authors: Lam, S.K., Poh, T.F., Ng, H.K., Hoe, S.Z.
Format: Article
Language:English
Published: Lippincott, Williams & Wilkins 2013
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Online Access:http://eprints.um.edu.my/10502/1/Gynura_procumbens_Causes_Vasodilation_by_Inhibiting.pdf
http://eprints.um.edu.my/10502/
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spelling my.um.eprints.105022014-10-13T01:37:17Z http://eprints.um.edu.my/10502/ Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions Lam, S.K. Poh, T.F. Ng, H.K. Hoe, S.Z. R Medicine (General) 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. Lippincott, Williams & Wilkins 2013 Article PeerReviewed application/pdf en http://eprints.um.edu.my/10502/1/Gynura_procumbens_Causes_Vasodilation_by_Inhibiting.pdf Lam, S.K. and Poh, T.F. and Ng, H.K. and Hoe, S.Z. (2013) Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions. Journal of Cardiovascular Pharmacology and Therapeutics, 61 (5). pp. 378-384. ISSN 0160-2446
institution Universiti Malaya
building UM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Malaya
content_source UM Research Repository
url_provider http://eprints.um.edu.my/
language English
topic R Medicine (General)
spellingShingle R Medicine (General)
Lam, S.K.
Poh, T.F.
Ng, H.K.
Hoe, S.Z.
Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions
description 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.
format Article
author Lam, S.K.
Poh, T.F.
Ng, H.K.
Hoe, S.Z.
author_facet Lam, S.K.
Poh, T.F.
Ng, H.K.
Hoe, S.Z.
author_sort Lam, S.K.
title Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions
title_short Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions
title_full Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions
title_fullStr Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions
title_full_unstemmed Gynura procumbens causes vasodilation by inhibiting angiotensin II and enhancing bradykinin actions
title_sort gynura procumbens causes vasodilation by inhibiting angiotensin ii and enhancing bradykinin actions
publisher Lippincott, Williams & Wilkins
publishDate 2013
url http://eprints.um.edu.my/10502/1/Gynura_procumbens_Causes_Vasodilation_by_Inhibiting.pdf
http://eprints.um.edu.my/10502/
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