Journal of Complementary and Integrative Medicine
Editor-in-Chief: Lui, Edmund
Ed. by Ko, Robert / Leung, Kelvin Sze-Yin / Saunders, Paul / Suntres, Zacharias
SCImago Journal Rank (SJR) 2015: 0.401
Source Normalized Impact per Paper (SNIP) 2015: 0.429
Impact per Publication (IPP) 2015: 1.255
Antihypertensive and Vasorelaxant Effects of Cinnamomum zeylanicum Stem Bark Aqueous Extract in Rats
1University of Dschang
2University of Douala
3University of Dschang
4University of Dschang
Citation Information: Journal of Complementary and Integrative Medicine. Volume 8, Issue 1, ISSN (Online) 1553-3840, DOI: https://doi.org/10.2202/1553-3840.1490, February 2011
- Published Online:
The present study was undertaken to evaluate the antihypertensive and vasorelaxant effects of Cinnamomum zeylanicum Blume stem bark aqueous extract in rats. The in vivo activities of the extract were evaluated on normotensive and three rat models of hypertension while the in vitro tests were assayed on rat isolated aorta rings. Acute intravenous injection of the extract (5, 10 and 20mg/kg) induced a significant reduction in mean arterial blood pressure in anaesthetised normotensive Wistar rats, salt-loaded hypertensive, L-NAME hypertensive and spontaneously hypertensive rats. Pre-treatment of rats with either propranolol or atropine significantly inhibited the hypotensive effects of the plant extract suggesting its possible action through the interferences with both cholinergic and sympathetic transmissions. Moreover, pre-treatment of rats with L-NAME inhibited the sustained plant antihypertensive effects, suggesting a possible active vasodilatation, which might be partly mediated by an endothelial l-arginine/nitric oxide pathway. In isolated rat aortic rings pre-contracted with KCl (60mM), the extract exhibited cumulative vasodilating effects, which were attenuated with either L-NAME, vascular endothelium removal or both tetraethylammonium and glibenclamide pre-treatments. The vasorelaxant effects may be involved in the extract antihypertensive mechanism, partially by increasing the endothelial nitric oxide and by activating the KATP channels in vascular smooth muscle.
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