A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression
A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression
复制标题
盐诱导的肾病脑反射激活肾素-血管紧张素系统并促进 CKD 进展
DOI：
10.1681/asn.2014050518
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发表时间：
2015-07-01
影响因子：
13.6
通讯作者：
Hou, Fan Fan
中科院分区：
文献类型：
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作者：
Cao, Wei;Li, Aiqing;Hou, Fan Fan
盐摄入促进慢性肾脏病进展的机制尚不明确。我们假设盐诱导的肾-脑反射激活肾素-血管紧张素轴以促进CKD。假手术组和5/6肾切除大鼠分别给予正常盐(0.4%)、低盐(0.02%)和高盐(4%)饲料喂养2周。5/6肾切除大鼠高盐增加肾脏NADPH氧化酶、炎症、血压和蛋白尿。此外，高盐激活肾内和大脑，而不是系统的肾素-血管紧张素轴，并增加这些大鼠肾交感神经和前脑神经元的活动。高盐组大鼠肾脏纤维化程度是低盐组的2.2倍，而侧脑室注射坦普尔、氯沙坦或可乐定可使肾纤维化程度分别降低65%、69%或59%，去神经或去传入分别可使肾纤维化程度降低43%或38%(均P
Salt intake promotes progression of CKD by uncertain mechanisms. We hypothesized that a salt-induced reno-cerebral reflex activates a renin-angiotensin axis to promote CKD. Sham-operated and 5/6-nephrectomized rats received a normal-salt (0.4%), low-salt (0.02%), or high-salt (4%) diet for 2 weeks. High salt in 5/6-nephrectomized rats increased renal NADPH oxidase, inflammation, BP, and albuminuria. Furthermore, high salt activated the intrarenal and cerebral, but not the systemic, renin-angiotensin axes and increased the activity of renal sympathetic nerves and neurons in the forebrain of these rats. Renal fibrosis was increased 2.2-fold by high versus low salt, but intracerebroventricular tempol, losartan, or clonidine reduced this fibrosis by 65%, 69%, or 59%, respectively, and renal denervation or deafferentation reduced this fibrosis by 43% or 38%, respectively (all P