首页> 美国卫生研究院文献>International Journal of Vascular Medicine >Vascular Reactivity Concerning Orthosiphon stamineus Benth-Mediated Antihypertensive in Aortic Rings of Spontaneously Hypertensive Rats
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Vascular Reactivity Concerning Orthosiphon stamineus Benth-Mediated Antihypertensive in Aortic Rings of Spontaneously Hypertensive Rats

机译:自发性高血压大鼠主动脉环上正方针刺亚目贝斯介导的降压反应的血管反应

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摘要

Orthosiphon stamineus Benth has been traditionally used to treat hypertension. The study aimed to investigate the vascular reactivity of water extract (WOS) and water : methanolic (1 : 1) extract (WMOS) of Orthosiphon stamineus Benth and AT1 receptors blocker in the mechanisms of antihypertensive mediated by α 1-adrenergic receptor and EDNO and PGI2 releases in the SHR aortic rings. SHR (230–280 g) were divided into four groups: control, WOS, WMOS, and losartan. After being fed orally for 14 days, the aorta was harvested and subjected to PE (10−9 to 10−5 M) and ACh (10−9 to 10−5 M) with and without L-NAME (100 µM) and indomethacin (10 µM), respectively. WOS, WMOS, and losartan significantly reduced the contractile responses to PE intact suggesting the importance of endothelium in vasorelaxation. Losartan significantly enhanced the ACh-induced vasorelaxation. L-NAME significantly inhibited the ACh-induced relaxation in all groups. Indomethacin enhanced ACh-induced vasorelaxation in WMOS. Collectively, Orthosiphon stamineus leaves extract reduced vasoconstriction responses by the alteration of α 1-adrenergic and AT1 receptors activities. The involvement of EDNO releases was clearly observed in this plant. In WOS, PGI2 releases might not participate in the ACh-induced vasorelaxation. However, in WMOS, enhancement of vasorelaxation possibly due to continuous release of PGI2.
机译:Orthosiphon stamineus Benth传统上用于治疗高血压。本研究旨在探讨邻位菊苣贝斯和AT1受体阻滞剂的水提取物(WOS)和水:甲醇(1:1)提取物(WMOS)的血管反应在α1-肾上腺素能受体和EDNO介导的降压机制中的作用。 PGI2在SHR主动脉环中释放。 SHR(230–280μg)分为四组:对照组,WOS,WMOS和氯沙坦。口服喂养14天后,收获主动脉并进行PE(10 -9 至10 -5 M)和ACh(10 −9 < / sup>至10 −5 M),分别带有和不带有L-NAME(100 µM)和消炎痛(10 µM)。 WOS,WMOS和氯沙坦完好无损地降低了对PE的收缩反应,表明内皮在血管舒张中的重要性。氯沙坦显着增强了ACh诱导的血管舒张。 L-NAME在所有组中均显着抑制ACh诱导的松弛。消炎痛增强了WMOS中ACh诱导的血管舒张。总的来说,Orthosiphon茎叶提取物通过改变α1-肾上腺素能和AT1受体的活性而减少了血管收缩反应。在该植物中清楚地观察到EDNO释放的参与。在WOS中,PGI2释放可能不参与ACh诱导的血管舒张。但是,在WMOS中,血管舒张的增强可能是由于PGI2的持续释放引起的。

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