The effect of acute Ang II blockade on renal function in rats with reduced nephron number was assessed in micropuncture studies. The Ang II receptor blocker, losartan, was administered at a dose of 10 mg i.v. at two intervals following five-sixths renal ablation. At eight weeks following ablation, Ang II blockade (Ang IIX) increased sodium excretion [UNaV, Ang IIX 2.2 +/- 0.4 mu Eq/min; time control (TC) 1.0 +/- 0.3 mu Eq/min; P < 0.05] but did not reduce mean arterial pressure (<(AP)over bar>, Ang IIX 142 +/- 6 mm Hg; TC 151 +/- 6 mm Hg), glomerular transcapillary pressure (Delta P, Ang IIX 50 +/- 1 mm Hg; TC 50 +/- 1 mm Hg), or urine albumin excretion (UAlbV: Ang IIX 149 +/- 18 mu g/min; TC 168 +/- 20 mu g/min). Similarly, at two weeks following ablation, Ang II blockade increased UNaV (Ang IIX 2.8 +/- 0.4 mu Eq/min; TC 0.5 +/- 0.2 mu Eq/min; P < 0.05) without reducing <(AP)over bar> (Ang IIX 132 +/- 6 mm Hg; TC 140 +/- 7 mm Hg), Delta P (Ang IIX 50 +/- 3 mm Hg; TC 48 +/- 2 mm Hg), or U-Alb,V (Ang IIX 32 +/- 3 mu g/min; TC 36 +/- 10 mu g/min). These findings indicate that within the remnant kidney, Ang II promotes sodium retention but does not have an acutely reversible effect on glomerular pressure or permselectivity.