Vasodilatatory effect and mechanism of CH2Cl2 extract of flos magnoliae on isolated rat thoracic aorta

AIM: To characterize the vasodilatatory effect of CH₂Cl₂ extract of flos magnoliae (CEF) on isolated rat thoracic aorta and to elucidate its possible mechanism. METHODS: The thoracic aorta was isolated from male Sprague-Dawley (SD) rats and the isometric tension of aortic rings with or without endothelium was measured. RESULTS: CEF (0.1-1 000 mg/L) produced concentration-dependent, endothelium-independent relaxations in phenylephrine (PE)-contracted aortic rings. The maximum relaxation induced by CEF was 78.68%±6.03% in endothelium intact rings and 64.98%±13.90% in endothelium removed rings while the forskolin (1 μmol/L)-induced vasodilation was obtained as 100%. The vasodilatatory effect of CEF was not statistically inhibited by 10 μmol/L glibenclamide (Glib), 3 mmol/L tetraethylammonium (TEA), 100 μmol/L BaCl₂ and 10 μmol/L 1H- -oxadiazole- -quinoxalin-1-one (ODQ) in the preparations without endothelium. The CEF pre-treatment significantly inhibited vasoconstrictions to angiotensin Ⅱ (AngⅡ), prostaglandin F_2α, (PGF_2α), dopamine (Dopa), vasopressin (Vaso), 5-hydroxytryptamine (5-HT) and PE by 91.31%, 82.11%, 95.32%, 90.53%, 72.22% and 83.63%, respectively (P<0.01). In Ca²⁺-free medium treated endothelium removed aortic ring, incubation with CEF at concentration of 82 mg/L significantly attenuated intracellular Ca²⁺ release by PE. In Ca²⁺-free + high potassium medium incubated aortic rings without endothelium, CEF (82 mg/L) markedly inhibited potassium-stimulated Ca²⁺-dependent contraction which was mainly due to Ca²⁺ influx (P<0.01).CONCLUSION: CEF induced vasorelaxation is mainly related to interfering intracellular calcium homeostasis by blocking Ca²⁺ influx and intracellular Ca²⁺ release.