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.
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