Supplemental Digital Content is available in the text. A key finding supporting a causal role of the immune system in the pathogenesis of hypertension is the observation that RAG1 knockout mice on a C57Bl/6J background (B6.Rag1−/−), which lack functional B and T cells, develop a much milder hypertensive response to Ang II (angiotensin II) than control C57Bl/6J mice. Here, we report that we never observed any Ang II resistance of B6.Rag1−/− mice purchased directly from the Jackson Laboratory as early as 2009. B6.Rag1−/− mice displayed nearly identical blood pressure increases monitored via radiotelemetry and hypertensive end-organ damage in response to different doses of Ang II and different levels of salt intake (0.02%, 0.3%, and 3% NaCl diet). Similarly, restoration of T-cell immunity by adoptive cell transfer did not affect the blood pressure response to Ang II in B6.Rag1−/− mice. Full development of the hypertension-resistant phenotype in B6.Rag1−/− mice appears to depend on the action of yet unidentified nongenetic modifiers in addition to the absence of functional T cells.

中文翻译：

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2009 年在杰克逊实验室产生的 B6.Rag1 基因敲除小鼠显示出对血管紧张素 II（血管紧张素 II）有强烈反应的野生型高血压表型

补充数字内容在文本中可用。支持免疫系统在高血压发病机制中起因果作用的一个关键发现是观察到缺乏功能性 B 和 T 细胞的 C57Bl/6J 背景 (B6.Rag1−/−) 上的 RAG1 敲除小鼠会发育得更温和对 Ang II（血管紧张素 II）的高血压反应高于对照 C57Bl/6J 小鼠。在这里，我们报告说，我们从未观察到早在 2009 年直接从杰克逊实验室购买的 B6.Rag1-/- 小鼠的任何 Ang II 抗性。 B6.Rag1-/- 小鼠显示出几乎相同的血压升高，通过无线电遥测和高血压结束- 响应不同剂量的 Ang II 和不同水平的盐摄入（0.02%、0.3% 和 3% NaCl 饮食）的器官损伤。相似地，通过过继细胞转移恢复 T 细胞免疫并不影响 B6.Rag1-/- 小鼠对 Ang II 的血压反应。除了缺乏功能性 T 细胞外，B6.Rag1-/- 小鼠的抗高血压表型的完全发展似乎还取决于尚未确定的非遗传修饰物的作用。