Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney
Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney
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DOI：
10.1152/ajprenal.00463.2012
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发表时间：
2013-04-01
影响因子：
4.2
通讯作者：
Rodriguez-Iturbe, Bernardo
中科院分区：
文献类型：
--
作者：
Franco, Martha;Tapia, Edilia;Rodriguez-Iturbe, Bernardo
Franco M、Tapia E、Bautista R、Pacheco U、Santamaria J、Quiroz Y、Johnson RJ、Rodriguez-Iturbe B。Am J Physiol肾脏Physiol 304：F982-F990,2013。2013年1月30日首次出版；doi：10.1152/ajprenal.00463.2012。-肾脏免疫细胞浸润是盐敏感型高血压的恒定特征。在灌胃一过性N-硝基-L-精氨酸甲酯(L-NAME)所致的SSHTN模型中，我们评价了肾脏炎症与压力性钠尿的关系。在停止L-NAME后1wk开始给予高盐(4%NaC l)饲料4wk的Wistar大鼠，测定压力钠排泄率。众所周知，与L名字相关的MMF的管理会阻止SSHTN的后续发展。对照组给予高盐饮食(n=12)和正常盐饮食(n=20)。SSHTN组大鼠炎症细胞因子表达增加，氧化应激增加。高血压的严重程度与肾小管间质免疫细胞和血管紧张素II表达细胞的数量直接相关(P<；0.0001)。在肾动脉压(RAP)分别为90、110、130和150毫米汞柱的情况下进行了血压钠尿的研究。各组肾小球滤过率相似且稳定，肾血流量明显减少。在RAP为130和150 mm Hg时，SSHTN组大鼠的尿钠排泄量显著减少(P<；0.05)，尿钠排泄量与肾小管间质炎症细胞(淋巴细胞和巨噬细胞)和血管紧张素Ⅱ表达细胞的数量呈负相关(P<；0.01)。
Franco M, Tapia E, Bautista R, Pacheco U, Santamaria J, Quiroz Y, Johnson RJ, Rodriguez-Iturbe B. Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney. Am J Physiol Renal Physiol 304: F982-F990, 2013. First published January 30, 2013; doi: 10.1152/ajprenal.00463.2012.-Immune cell infiltration of the kidney is a constant feature in salt-sensitive hypertension (SSHTN). We evaluated the relationship between the renal inflammation and pressure natriuresis in the model of SSHTN that results from transient oral administration of N omega-nitro-L-arginine methyl ester (L-NAME). Pressure natriuresis was determined in Wistar rats that received 4 wk of a high-salt (4% NaCl) diet, starting 1 wk after stopping L-NAME, which was administered alone (SSHTN group, n = 17) or in association with mycophenolate mofetil (MMF; MMF group, n = 15). The administration of MMF in association with L-NAME is known to prevent the subsequent development of SSHTN. Control groups received a high (n = 12)- and normal (0.4%)-salt diet (n = 20). Rats with SSHTN had increased expression of inflammatory cytokines and oxidative stress. The severity of hypertension correlated directly (P < 0.0001) with the number of tubulointerstitial immune cells and angiotensin II-expressing cells. Pressure natriuresis was studied at renal arterial pressures (RAPs) of 90, 110, 130, and 150 mmHg. Glomerular filtration rate was similar and stable in all groups, and renal blood flow was decreased in the SSHTN group. Significantly decreased natriuresis (P < 0.05) was found in the SSHTN group at RAPs of 130 and 150 mmHg, and there was an inverse correlation (P < 0.01) between the urinary sodium excretion and the number of tubulointerstitial inflammatory cells (lymphocytes and macrophages) and cells expressing angiotensin II. We conclude that tubulointerstitial inflammation plays a key role in the impairment of pressure natriuresis that results in salt-dependent hypertension in this experimental model.