The present study examined the effect of an angiotensin II AT₁ or AT₂ receptor antagonist on the impairment of the pressure diuresis and natriuresis response produced by nitric oxide (NO) synthesis blockade.N ^ω-nitro-l-arginine methyl ester (l-NAME, 37 nmol ⋅ kg⁻¹ ⋅ min⁻¹) lowered renal blood flow and reduced the slopes of the pressure diuresis and natriuresis responses by 44 and 40%, respectively. Blockade of AT₁ receptors with valsartan increased slightly sodium and water excretion at low renal perfusion pressure (RPP). Blockade of AT₂ receptors with PD-123319 had no effect on renal function. The administration of valsartan or PD-123319 to rats given l-NAME had no effect on the renal vasocontriction induced by NO synthesis blockade. In addition, in rats givenl-NAME, valsartan elevated baseline excretory values at all RPP studied, but it had no effect on the sensitivity of the pressure diuresis and natriuresis response. However, the administration of PD-123319 tol-NAME-pretreated rats shifted the slopes of the pressure diuresis and natriuresis responses toward control values, indicating that the impairment produced by NO synthesis blockade on pressure diuresis is dependent on the activation of AT₂ angiotensin receptors.