In angiotensin II (Ang II) dependent hypertension, there is an AT1 receptor dependent amplification mechanism enhancing intrarenal angiotensinogen (AGT) formation and secretion into the tubular fluid. To evaluate the role of increased arterial pressure, AGT mRNA, protein expression, and urinary AGT (uAGT) excretion and tissue injury were assessed in both kidneys of 2-kidney, 1-clip (2K1C) Sprague Dawley hypertensive rats subjected to left renal arterial clipping (0.25 mm gap). By 18-21 days, systolic arterial pressure increased to 180±3 mmHg, and uAGT increased. Water intake, body weights, 24 hr urine volumes and sodium excretion were similar. In separate measurements of renal function in anesthetized rats, renal plasma flow and glomerular filtration rate (GFR) were similar in clipped and non-clipped kidneys and not different from those in sham rats indicating that the perfusion pressure to the clipped kidneys remained within the autoregulatory range. The non-clipped kidneys exhibited increased urine flow and sodium excretion. The uAGT excretion was significantly greater in non-clipped kidneys compared to clipped and sham kidneys. AGT mRNA was 2.15 fold greater in the non-clipped kidneys compared to sham (1.0±0.1) or clipped kidneys (0.98±0.15). AGT protein levels were also greater in the non-clipped kidneys. The non-clipped kidneys exhibited greater glomerular expansion and immune cell infiltration, medullary fibrosis, and cellular proliferation than the clipped kidneys. Because both kidneys have elevated Ang II levels, the greater tissue injury in the non-clipped kidneys indicates that an increased arterial pressure synergizes with increased intrarenal Ang II to stimulate AGT production and exert greater renal injury.