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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 513068, 7 pages
Research Article

Cinnamomi ramulus Ethanol Extract Exerts Vasorelaxation through Inhibition of Influx and Release in Rat Aorta

Department of Physiology, College of Oriental Medicine, Dongguk University, Gyeongju 780-714, Republic of Korea

Received 4 March 2011; Accepted 15 May 2011

Academic Editor: David Baxter

Copyright © 2012 Yun Hwan Kang and Heung Mook Shin. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Contraction of vascular smooth muscle cells depends on the induction of cytosolic calcium ion (Ca2+) due to either Ca2+ influx through voltage-gated Ca2+ channels or to receptor-mediated Ca2+ release from the sarcoplasmic reticulum. The present study investigated the vasorelaxation effect of Cinnamomi ramulus ethanol extract (CRE) and the possible mechanisms in rat aorta. CRE (0.1 mg/mL) relaxed vasoconstriction induced by phenylephrine (PE; 1 μM) and angiotensin II (5 μM). Preincubation with CRE significantly reduced the rat aortic contraction by addition of CaCl2 in Ca2+-free Krebs solution and FPL64176 (10 μM). Pretreatment with nifedipine (100 μM) or verapamil (1 μM) significantly reduced the CRE-mediated vasorelaxation of PE-induced vascular contraction. In addition, CRE also relaxed the vascular contraction caused by m-3M3FBS (5 μg/mL), but U73122 (10 μM) significantly inhibited the vasorelaxation of PE precontracted aortic rings. Furthermore, CRE significantly reduced the magnitude of PE- and caffeine (30 mM)-induced transient contraction. In vascular strips, CRE downregulated the expression levels of phosphorylated PLC and phosphoinositide 3-kinase elevated by PE or m-3M3FBS. These results suggest that CRE relaxes vascular smooth muscle through the inhibition of both Ca2+ influx via L-type Ca2+ channel and inositol triphosphate-induced Ca2+ release from the sarcoplasmic reticulum.