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首页> 外文期刊>American Journal of Physiology >Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism.
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Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism.

机译：高尿酸血症通过一种与血压无关的机制诱发大鼠原发性肾小动脉病变。

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Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system.
机译：高尿酸血症与高血压和血管疾病有关，但是这是否代表因果关系或表观现象尚不清楚。我们最近报道了大鼠轻度高尿酸血症的模型，可导致血压升高和轻度肾纤维化。在这项研究中，我们检查了高尿酸血症对肾血管的影响。喂食2％草酸和低盐饮食连续7周的大鼠出现轻度高尿酸血症（1.8 vs. 1.4 mg / dl，P <0.05），高血压[147 vs. 127 mmHg收缩压（PBP），P <0.05] ，以及传入小动脉增厚，内侧面积增加35％（P <0.05）。别嘌醇或苯齐那达酮可预防高尿酸血症，高血压和小动脉病变。尽管控制血压，氢氯噻嗪治疗仍不能预防高尿酸血症或动脉粥样硬化。相比之下，依那普利和氯沙坦均可以预防动脉病变和高血压。尿酸还可以直接刺激体外血管平滑肌细胞的增殖，而氯沙坦可以部分抑制这种增殖。因此，高尿酸血症在大鼠中诱发了与血压无关并且涉及肾素-血管紧张素系统的肾动脉病变。

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