Our recent studies have demonstrated that salt excess in the spontaneously hypertensive rat (SHR), produces a modestly increased arterial pressure while promoting marked myocardial fibrosis and structural damage associated with altered coronary hemodynamics and ventricular function. The present study was designed to determine the efficacy of angiotensin II type 1 receptor blocker (ARB) in prevention of pressure increase and development of target organ damage from high dietary salt intake. Eight week-old SHR were given 8% salt diet for 8 weeks; their age and gender matched controls received standard chow. Some of the salt-loaded rats were treated concomitantly with ARB (candesartan; 10 mg/kg/day). The ARB failed to reduce the salt-induced rise in pressure whereas it significantly attenuated left ventricular (LV) remodeling (mass, wall thicknesses), myocardial fibrosis (hydroxyproline concentration and collagen volume fraction), and development of LV diastolic dysfunction as shown by longer isovolumic relaxation time, decreased ratio of peak velocity of early to late diastolic waves, and slower LV relaxation (dP/dT_min/LVP _max). Without affecting the increased pulse pressure by high salt intake, the ARB prevented the salt-induced deterioration of coronary and renal hemodynamics, but not the arterial stiffening or hypertrophy (pulse wave velocity and aortic mass index). Additionally, candesartan prevented salt-induced increase in kidney mass index and proteinuria. In conclusion, the ARB given concomitantly with dietary salt excess ameliorated salt-related structural and functional cardiac and renal abnormalities in SHR without reducing arterial pressure. These data clearly demonstrated that angiotensin II (via AT₁ receptors), at least in part, participated importantly in the pressure independent effects of salt excess on target organ damage of hypertension.