Abstract 002: Activation of AT1 receptors on Dendritic Cells Restrains Angiotensin II-Dependent Hypertension Through a CCR7-dependent Mechanism

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2014-11, Vol.64 (Suppl_1 Suppl 1), p.A002-A002
• Main Authors: zhang, Jiandong, Karlovich, Norah S, Griffiths, Robert, crowley, Steven D
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.64.suppl_1.002

Dendritic cells (DCs) trigger an adaptive immune response by presenting processed antigens to T lymphocytes. Given the emerging importance of adaptive immunity in hypertension, we posited that DCs may sample neoantigens in the kidney in order to prime pro-hypertensive T cells. Using CD11c-Cre mT/mG mice in which DCs fluoresce green, we detected robust green signals within the kidney after 2 wks of angiotensin (Ang) II-induced hypertension, confirming infiltration of DCs into the hypertensive kidney. As activation of type 1 angiotensin (AT1) receptors on other immune cell lineages has been shown to alter inflammatory responses, we explored the role of the DC AT1 receptor in blood pressure regulation by generating mice with DC-specific deletion of the AT1A receptor (CD11c Cre+ Agtr1aflox/flox = DC KO) and littermate controls (Agtr1aflox/flox = WT). Compared to WTs, the DC KOs had an ≈87% reduction in AT1A receptor mRNA expression in DCs (p