Jump to Main Content
Cellular mechanisms underlying Hyperin-induced relaxation of rat basilar artery
- Fan, Yi-Fei, Chen, Zhi-Wu, Guo, Yan, Wang, Qi-Hai, Song, Biao
- Fitoterapia 2011 v.82 no.4 pp. 626-631
- Abelmoschus, endothelium, flavonols, glass, indomethacin, membrane potential, microscopy, myocytes, nitric oxide, nitric oxide synthase, potassium channels, prostacyclin, prostaglandin synthase, rats, smooth muscle
- BACKGROUND AND AIM: Hyperin, a flavonol compound extracted from the Chinese herb Abelmoschus manihot L. Medic, is reported to exert protective actions in cerebral ischemic injury. The specific aim of the present study was to study the relaxation of Hyperin in rat isolated basilar artery and identify the underlying cellular mechanisms. METHODS: Rat isolated basilar artery segments were cannulated and perfused while being superfused with PSS solution. Vessel images were recorded by video microscopy and diameters measured. Membrane potential was recorded using glass microelectrodes to evaluate the basilar artery smooth muscle cell hyperpolarization. RESULTS: Perfusion of Hyperin (1~100μM) elicited a concentration-dependent relaxation of basilar artery segments preconstricted with 0.1μM U46619. The response was significantly inhibited by the removal of the endothelium. Hyperin also elicited marked and concentration-dependent hyperpolarization of smooth muscle cells. 30μM nitro-L-arginine (an inhibitor of nitric oxide synthase) and indomethacin (an inhibitor of cyclooxygenase), partially inhibited Hyperin-induced relaxation and hyperpolarization leaving an attenuated, but significant, endothelium-dependent relaxation and hyperpolarization. This remaining effect was almost completely blocked by 1mM tetraethylammonium (an inhibitor of Ca²⁺-activated K⁺ channels), or by 100μM DL-propargylglycine, an inhibitor of cystathionine-γ-lyase (a synthase of the endogenous H₂S). CONCLUSION: These findings show that Hyperin produces significant hyperpolarization in rat basilar artery smooth muscle cells and relaxation through both endothelium-dependent and endothelium-independent mechanisms. The underlying mechanisms appeared to be multi-factorial involving nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). Our data further suggest that endogenous H₂S is a component of the EDHF-mediated hyperpolarization and relaxation to Hyperin.