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Total Flavones of Rhododendra-induced EDHF Responses in the Cerebral Basilar Artery of Rat Subjected to Global Cerebral Ischemia Reperfusion

Author: HanLiLi
Tutor: ChenZhiWu
School: Anhui Medical University,
Course: Pharmacology
Keywords: TFR endothelium-derived hyperpolarizing factor basilar artery hydrogen sulfide cerebral ischemia reperfusion vasorelaxation hyperpolarization
CLC: R741
Type: Master's thesis
Year: 2011
Downloads: 20
Quote: 0
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Abstract


The vascular endothelium releases endothelium-derived relaxing factors in response to some agonists or physical stimuli that mediate relaxation. These factors include nitric oxide （NO）, prostacyclin （PGI2）, and several factors called endothelium-derived hyperpolarizing factors （EDHFs）. At present, the role of EDHF has been researched in various peripheral vascular beds including coronary artery of human and dog , mesenteric artery of rats.Total flavones of rhododendra （TFR） was extracted from the flower of total flavones of Rhododendra. The essential components of TFR are hyperin, quercetin and other flavonoids. It has been preliminary assessed to be of protection against myocardial and cerebral ischemia. In this study, it was studied that EDHF-mediated responses of relaxation and hyperpolarization of vascular smooth muscle cell （VSMC） induced by TFR in rat cerebral basilar artery （CBA） subjected to cerebral ischemia/reperfusion （I/R） .Purpose:1. To study the EDHF-mediated hyperpolarization of VSMC and vasorelaxtion relaxation induced by TFR in rat CBA subjected I/R.2. To investigate the effects of TFR on outwardand K+ currents in rat CBA VSMC.Method:1. Cerebral ischemia reperfusion was induced by 4-vessle occlusion （4-VO） in rat.2. Isolated rat CBA segmnts were suspended in baths containing PSS solution, the relaxation was observed by using measurement of vessel diameter.3. Transmembrane potentials were recorded to evaluate the hyperpolarization effects in rat CBA VSMC. 4. Whole-cell patch clamp recording was used to measure the Ca2+-activated potassium （Kca） current in rat CBA VSMC.Results:1. In the presence of 3×10-5 mol/L Nω-nitro-L–arginine-methyl-ester （L-NAME, an inhibitor of nitric oxide synthase） and 1×10-5 mol/L indomethacin （Indo, an inhibitor of PGI2 synthesis）, the globa cerebral I/R markedly enhanced 1×10-7 1×10-5 mol/L acetylcholine-elicited hyperpolarization of RMP of VSMC and vasorelaxation in rat CBA,respetively.2. In the presence of L–NAME and Indo, 11 2700 mg/L TFR induced significant and dose-dependent hyperpolarization of RMP of VSMC and vasorelaxation in rat CBA subjected to global cerebral I/R.3. The hyperpolarization and relaxation were obviously inhibited by tetraethylammonium （an inhibitor of IKCa at 1 mmol/L） and 1×10-4 mol/L DL-propargylglycine, an inhibitor of endogenous hydrogen sulfide （H2S） synthase.4. 3002700mg/L TFR markedly enhanced the Ca2+-activated potassium （Kca） current in rat CBA VSMC.Conclusions:1. Global cerebral I/R could enhance the non-NO-non-PGI2–mediated responses of hyperpolarization and vasorelaxation in rat CAB.2. In rat CAB subjected to global cerebral I/R, TFR significantly induced EDHF-mediated the responses of hyperpolarization and relaxation, and the response may be related to endogenous H2S.

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