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

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 μM) and angiotensin II (5 μM). Preincubation with CRE significantly reduced the rat aortic contraction by addition of CaCl(2) in Ca(2+)-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 Ca(2+) influx via L-type Ca(2+) channel and inositol triphosphate-induced Ca(2+) release from the sarcoplasmic reticulum.