Fig. 8.

Mice treated with CCR2 inhibitor experienced sustained hypertension despite attenuation of renal injury. Systolic tail-cuff blood pressure measurements (A) and plasma renin activity (B) of RAS mice treated with CCR2 inhibitor (RS-102895; n = 9 mice) or vehicle (water; n = 12 mice) are shown. Plasma renin activity was assessed by production of angiotensin 1. C and D: gene expression changes in renin (Ren1; C) and angiotensinogen (Agt; D) in whole kidney homogenates from the stenotic kidneys of mice with sham surgery (n = 5 mice) or mice with RAS surgery that were treated with either CCR2 inhibitor or vehicle. Values are means ± SE normalized against 18S transcript and expressed as fold-increase relative to the 28-day sham expression.