Transient stimulation (4–8 weeks of age) of the renin angiotensin aldosterone system (RAAS) permanently increases blood pressure (BP) in young transgenic rats with inducible hypertension. The chronic elevation in BP is associated with the induction of irreversible changes in renal structure and function. To identify the responsible RAAS components that mediate this phenotype, we tested if concomitant administration of an angiotensin II receptor blocker (ARB) during transient RAAS stimulation (TRS) could prevent the development of permanently elevated BP and end-organ damage. Studies were performed in Cyp1a1 Ren2 transgenic rats with inducible hypertension. These rats harbor a construct for the production of mouse renin which becomes activated when indole-3 carbinol (I3C) is added to the diet. Experimental rats received 0.3% I3C-treatment with either an ARB (losartan: 20mg/kg/day) or vehicle between 4–8 weeks of age via a subcutaneously implanted osmotic minipump. Cyp1a1 Ren2 rats without I3C-treatment, with or without losartan, served as controls. Intra-arterial BP was determined at 4, 8, 12 and 20 weeks of age. Additionally, renal vascular resistance RVR was determined. Data are presented as mean ± SEM. At 8 weeks of age TRS rats demonstrate fulminant hypertension (Mean Arterial Pressure (MAP) of 170±9 mmHg versus 126±2 mmHg). Treatment with losartan had no effect on BP in the control rats (123±3mmHg), whereas BP was completely restored to baseline values in the TRS rats (126±3mmHg). At 20 weeks of age, i.e. 12 weeks after TRS, I3C-treated rats without losartan still demonstrated elevated MAP (152±10 mmHg versus 123±2 mmHg), whereas BP of losartan treated TRS rats remained at control levels (119±2 mmHg). This study shows that TRS induced sustained hypertension can be completely prevented by an ARB suggesting that AT1R activation is the main contribution to the irreversible renal damage in young Cyp1a1 Ren2 transgenic rats.