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首页> 外文期刊>Life sciences >Angiotensin II type 1 receptor blockade protects endothelium-derived hyperpolarising factor-mediated relaxation in a rat model of monoarthritis
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Angiotensin II type 1 receptor blockade protects endothelium-derived hyperpolarising factor-mediated relaxation in a rat model of monoarthritis

机译：血管紧张素II 1型受体阻滞在单关节炎模型中保护内皮源性超极化因子介导的舒张

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Aims Rheumatoid arthritis (RA) is associated with high cardiovascular mortality. Impaired endothelial cell (EC) function and elevated angiotensin II levels may be central to the link between vascular dysfunction and RA. Here we investigated the action of angiotensin type 1 receptor (AT1R) blockade on endothelium-dependent relaxation of the isolated saphenous artery in a rat model of monoarthritis. Main Methods Adjuvant arthritis was induced in rats with and without prophylactic losartan (AT1R antagonist) treatment. Vehicle-treated rats were used as controls. Wire myography was employed to investigate EC function of isolated rings of saphenous artery. Key Findings EC-dependent relaxation in arteries from non-inflamed control rats was mediated by both nitric oxide (NO) and endothelium-derived hyperpolarising factor (EDHF) with the EDHF response dependent principally on functional myoendothelial gap junctions. While NO-dependent relaxation remained unaffected, the EDHF-mediated response was abolished in arteries from arthritic rats (P < 0.001), however, substantial protection (approximately 50%) of the EDHF-relaxation was found in arthritic rats treated with losartan (P < 0.01). Thus, the attenuated EDHF response found in the saphenous artery of arthritic rats was significantly reversed by AT1R blockade. Significance These results suggest a key role for the angiotensin system in the EC dysfunction found in chronic joint inflammation and highlights AT1R as a potential therapeutic target to redress the vascular impairment and mortality associated with RA.
机译：目的类风湿关节炎（RA）与高心血管死亡率相关。内皮细胞（EC）功能受损和血管紧张素II水平升高可能是血管功能障碍与RA之间联系的中心。在这里，我们研究了单关节炎的大鼠模型中1型血管紧张素受体（AT1R）阻滞对孤立大隐动脉内皮依赖性舒张的作用。主要方法在有和没有预防性氯沙坦（AT1R拮抗剂）治疗的大鼠中诱发佐剂性关节炎。媒介物处理的大鼠用作对照。线肌成像被用来研究隐性大动脉分离环的EC功能。主要发现一氧化氮（NO）和内皮源性超极化因子（EDHF）均可介导非炎症对照组大鼠的EC依赖性舒张，而EDHF反应主要取决于功能性肌内皮间隙连接。尽管NO依赖性舒张功能未受到影响，但关节炎大鼠动脉中的EDHF介导的反应被消除了（P <0.001），但是，在使用氯沙坦（P <0.01）。因此，在关节炎大鼠的大隐动脉中发现的减弱的EDHF反应被AT1R阻断显着逆转。意义这些结果表明，血管紧张素系统在慢性关节炎症中发现的EC功能障碍中起关键作用，并强调AT1R是解决与RA相关的血管损伤和死亡率的潜在治疗靶标。

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