首页> 美国卫生研究院文献>International Journal of Hypertension >Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
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Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats

机译:自发性高血压大鼠阻力动脉中流量(剪切应力)介导的重塑的时间变化

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摘要

Hypertension is a major risk factor for cardiovascular disorders. As flow-mediated outward remodeling has a key role in postischemic revascularization, we investigated this remodeling in mesenteric resistance arteries of normotensive (WKY) and spontaneously hypertensive rats (SHRs) aged 3 to 9 months. Sequential ligation of mesenteric resistance arteries allowed modifying blood flow in vivo, thus exposing arteries to low, normal, or high flow. After 1, 3, 8, or 24 weeks, arteries were isolated for in vitro study. High flow (HF) induced outward hypertrophic remodeling in WKY rats after 1 week and persisted until 24 weeks without change in wall to lumen ratio. In SHRs, diameter increase was delayed, occurring only after 3 weeks. Nevertheless, it was reduced at 8 weeks and no longer significant after 24 weeks. In parallel, media cross-section area increased more with time in SHRs than in WKY rats and this was associated with increased contractility and oxidative stress with decreased NO-dependent relaxation. Low flow induced progressive inward remodeling until 24 weeks in both strains with excessive hypertrophy in SHRs. Thus, a chronic increase in flow induced transitory diameter expansion and long-lasting hypertrophy in SHRs. This could contribute to the higher susceptibility of hypertensive subjects to ischemic diseases.
机译:高血压是心血管疾病的主要危险因素。由于血流介导的向外重塑在缺血后血运重建中具有关键作用,因此我们在3到9个月大的正常血压(WKY)和自发性高血压大鼠(SHRs)的肠系膜阻力动脉中研究了这种重塑。肠系膜阻力动脉的顺序结扎可改变体内的血流,从而使动脉暴露于低,正常或高流量。在1、3、8或24周后,分离出动脉进行体外研究。高流量(HF)诱导WKY大鼠在1周后向外肥大重塑,并持续到24周,而管壁比没有变化。在SHR中,直径增加被延迟,仅在3周后发生。尽管如此,它在第8周时减少了,在24周后不再显着。同时,与WKY大鼠相比,SHRs中的培养基横截面积随时间增加更多,这与收缩力和氧化应激增加以及NO依赖性舒张减少有关。在两个SHRs过度肥大的菌株中,低流量诱导进行性向内重塑直至24周。因此,流量的慢性增加导致SHRs的瞬时直径扩大和长期肥大。这可能导致高血压受试者对缺血性疾病的敏感性更高。

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