[Endothelium-dependent vasorelaxation effects induced by apigenin on the thoracic aorta of rats and its possible mechanism].

OBJECTIVE: To investigate the vasorelaxant effect and mechanism of apigenin. METHODS: Rats were anesthetized with 1% sodium pentobarbital (i. p.) and killed by exsanguination. The thoracic aorta was isolated and cut into 3-4 mm rings and suspended in an organ bath filled with 20 ml Kreb solution which was maintained at 37 degrees C and ventilated continuously with 95% O2 and 5% CO2. The contraction was measured with a multichannel acquisition and analysis system (BIO-PAC MP150, America). Related studies were conducted on the effect of apigenin on the contraction induced by phenylephrine (PE) and role of endothelium, K+ channel as well as Ca2+ channel in PE-induced relaxation. RESULT: Apigenin had no effect on the basal tension in rat aortic rings. Apigenin can relax PE pre-contracted rings in both endothelium-intact aortic and endothelium-denuded aortic in a dose-dependent manner, with the effect of endothelium-intact aortic significantly stronger than that of endothelium-denuded aortic (P < 0.05). Pre-incubation of endothelium-intact rings with L-NAME and methylene blue significantly reduced apigenin-induced relaxation (P < 0.05). However, indomethacin did not significantly affect the apigenin-induced relaxation in endothelium-intact rings (P > 0.05). 4-AP, 5-HD, TEA as well as BaCl2 significantly inhibited apigenin-induced relaxation in endothelium-denuded rings pre-contracted by PE (P < 0.05). In the K(+)-free solution, apigenin can significantly inhibit PE pre-contracted aortic rings (P < 0.05). In the Ca2(+)-free solution plus PE, cumulative addition of CaCl2 induced a stepwise tension increase of aortic rings. Pretreated with apigenin significantly attenuated CaCl2 induced contraction. CONCLUSION: Apigenin induces both endothelium-dependent and independent relaxation. NO and cGMP are involved in the endothelium-dependent relaxation, inhibition of voltage-dependent or receptor-operate Ca2+ channel or extracellular Ca2+ influx and activation of K channel contribute in part to the endothelium-independent relaxation by apigenin.