1. B6.Rag1 Knockout Mice Generated at the Jackson Laboratory in 2009 Show a Robust Wild-Type Hypertensive Phenotype in Response to Ang II (Angiotensin II).
- Author
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Seniuk A, Thiele JL, Stubbe A, Oser P, Rosendahl A, Bode M, Meyer-Schwesinger C, Wenzel UO, and Ehmke H
- Subjects
- Animals, Disease Models, Animal, Hypertension genetics, Male, Mice, Mice, Knockout, Angiotensin II, Homeodomain Proteins genetics, Hypertension chemically induced, Phenotype
- Abstract
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- ), 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.- Published
- 2020
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