Abstract 613: Mitochondrial Hydrogen Peroxide In T Cell Activation In Hypertension

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2014-09, Vol.64 (suppl_1)
• Main Authors: Nazarewicz, Rafal R, Saleh, Mohamed A, Wu, Jing, Dikalov, Sergey, Harrison, David G
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.64.suppl_1.613

Abstract only Substantial evidence demonstrates that mitochondrial reactive oxygen species and adoptive immunity are critical in the development of hypertension. Our initial observations indicated that T cells isolated from hypertensive mice produced more cellular and mitochondrial hydrogen peroxide (H2O2) compared to those from normotensive animals, 98% and 48% respectively. We hypothesized that mitochondrial H2O2 plays a regulatory role in T cell activation in hypertension. We used RAG1-/- male mice that lack lymphocytes and modulated mitochondrial H2O2 by adoptive transfer of T cells with various mitochondrial H2O2 levels. RAG1-/- mice received T cells from wild type mice (RAG1-/-+WT) or mice expressing catalase in mitochondria (RAG1-/-+mCat). Adoptive transfer of T cells was performed 3 weeks prior to Ang II infusion (490 ng/kg/min). Our data show that inhibition of mitochondrial H2O2 specifically in T cells prevents hypertension. When challenged with angiotensin II, systolic BP in RAG1-/-+WT mice rose to 174 mmHg (+/-7.7) which was similar to values observed in WT mice (173 mmHg +/-12). However, scavenging mitochondrial H2O2 in T cells significantly (P