Cinnamomi ramulus Ethanol Extract Exerts Vasorelaxation through Inhibition of Ca2+ Influx and Ca2+ Release in Rat Aorta. (13th July 2011)

• Record Type: Journal Article
• Authors: Kang, Yun Hwan; Shin, Heung Mook
• Other Names: Baxter David Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2012(2012)
• Publication Date: 2011-07-13
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2012/513068
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Contraction of vascular smooth muscle cells depends on the induction of cytosolic calcium ion (Ca 2+ ) due to either Ca 2+ influx through voltage-gated Ca 2+ channels or to receptor-mediated Ca 2+ 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 μ M) and angiotensin II (5 μ M). Preincubation with CRE significantly reduced the rat aortic contraction by addition of CaCl2 in Ca 2+ -free Krebs solution and FPL64176 (10 μ M). Pretreatment with nifedipine (100 μ M) or verapamil (1 μ M) significantly reduced the CRE-mediated vasorelaxation of PE-induced vascular contraction. In addition, CRE also relaxed the vascular contraction caused by m-3M3FBS (5 μ g/mL), but U73122 (10 μ M) 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 Ca 2+ influx via L-type Ca 2+ channel and inositol triphosphate-induced Ca 2+ release from the sarcoplasmic reticulum.