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首页> 外文期刊>American Journal of Physiology >Rag1-null Dahl SS rats reveal that adaptive immune mechanisms exacerbate high protein-induced hypertension and renal injury
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Rag1-null Dahl SS rats reveal that adaptive immune mechanisms exacerbate high protein-induced hypertension and renal injury

机译：Rag1-null dahl ss大鼠揭示了适应性免疫机制加剧了高蛋白质诱导的高血压和肾损伤

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The present study, performed in Dahl salt-sensitive (SS) and SS-Rag1?/? rats lacking T and B lymphocytes, tested the hypothesis that immune cells amplify salt-sensitive hypertension and kidney damage in response to a high-protein diet. After being weaned, SS and SS-Rag1?/? rats were placed on an isocaloric, 0.4% NaCl diet containing normal (18%) or high (30%) protein. At 9 wk of age, rats were switched to a 4.0% NaCl diet containing the same amount of dietary protein and maintained on the high-salt diet for 3 wk. After being fed the high-salt diet, SS rats fed high protein had amplified hypertension and albumin excretion (158.7?±?2.6 mmHg and 140.8?±?16.0 mg/day, respectively, means ± SE) compared with SS rats fed normal protein (139.4?±?3.6 mmHg and 69.4?±?11.3 mg/day). When compared with the SS rats, SS-Rag1?/? rats fed high protein were protected from exacerbated hypertension and albuminuria (142.9?±?5.8 mmHg and 66.2?±?10.8 mg/day). After 3 wk of the high-salt diet, there was a corresponding increase in total leukocyte infiltration (CD45+) in the kidneys of both strains fed high-protein diet. The SS-Rag1?/? rats fed high-protein diet had 74–86% fewer CD3+ T lymphocytes and CD45R+ B lymphocytes infiltrating the kidney versus SS rats, but there was no difference in the infiltration of CD11b/c+ monocytes and macrophages, suggesting that the protective effects observed in the SS-Rag1?/? rats are specific to the reduction of lymphocytes. With the SS-Rag1?/? rats utilized as a novel tool to explore the effects of lymphocyte deficiency, these results provide evidence that adaptive immune mechanisms contribute to the exacerbation of salt-induced hypertension and renal injury mediated by increased dietary protein intake.
机译：本研究，在DAHL盐敏感（SS）和SS-RAG1中进行？/？缺乏T和B淋巴细胞的大鼠，测试了免疫细胞扩增盐敏高血压和肾脏损伤的假设，以应对高蛋白质饮食。断奶后，ss和ss-rag1？/？将大鼠置于异蜂米上，含有正常（18％）或高（30％）蛋白的0.4％NaCl饮食。在9周龄，大鼠切换到含有相同量的膳食蛋白的4.0％NaCl饮食，并保持在高盐饮食中3周。喂养高盐饮食后，喂养高蛋白质的SS大鼠具有扩增的高血压和白蛋白排泄（分别为158.7Ω·±2.6mmHg和140.8？±16.0mg /天，平均值±SE）与喂养正常蛋白相比（139.4？±3.6 mmHg和69.4？±11.3毫克/天）。与SS RATS相比，SS-RAG1？/？喂养高蛋白质的大鼠免受加剧的高血压和白蛋白尿（142.9〜±5.8mmHg和66.2？±10.8毫克/天）。经过3周的高盐饮食后，两种菌株喂养高蛋白质饮食的肾脏总白细胞浸润（CD45 +）的相应增加。 ss-rag1？/？喂养高蛋白饮食的大鼠较少的CD3 + T淋巴细胞和CD45R + B淋巴细胞浸润肾脏，但CD11b / c +单核细胞和巨噬细胞的浸润没有差异，表明在该CD11b / c +单核细胞和巨噬细胞的浸润中缺血ss-rag1？/？大鼠特异于减少淋巴细胞。与SS-RAG1？/？用作新型工具的大鼠用于探讨淋巴细胞缺乏的影响，这些结果提供了据证据表明，适应性免疫机制有助于加剧盐诱导的高血压和通过增加膳食蛋白摄入介导的肾损伤。

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