Angiotensin II‐induced hypertension results in an oligioclonal T cell receptor expansion in mouse kidney

The purpose of this investigation was to determine if T cells that infiltrate the kidney and promote hypertension exhibit a mono‐ or polyclonal T cell receptor (TCR) phenotype. We produced hypertension in C57Bl/6 mice by infusion of angiotensin II (2 week, 490 ng/kg/min) and used vehicle infused mice as controls. PCR was employed to amplify the 24 TCR Vβ families in CD4 and CD8 cells isolated from the kidney. PCR products were subjected to fragment analysis to determine TCR Vβ transcript length. CD8 TCR length profiles for Vβ 5.1, 8.1, 8.3, and 17 and CD4 Vβ 8.2, 14 and 16 were significantly different (Dirchelet distribution, p ≤ 0.05) with angiotensin II. To determine if mice with an altered TCR phenotype are protected against hypertension, OT1 mice, which have CD8 cells with a transgenic TCR specific for ovaalbumin, were infused with angiotensin II or vehicle. Blood pressure was measured by telemetery. After 2 weeks OT1 mice infused with angiotensin II exhibited increased systolic blood pressure compared to controls (171 ± 10 vs. 117 ± 15 mmHg, mean ± SEM). Analysis of kidney CD8 T cells revealed that OT1 mice possessed a dominant a Vβ 5 TCR specific to ovaalbumin as well as all other Vβ families with the exception of Vβ 17. Overall, these data suggest that angiotensin II infusion results in oligioclonal T cell expansion and that these cells may mediate hypertension.