Determinants of glomerular ultrafiltration were studied by micropuncture in clamped kidneys of one-kidney Goldblatt rats (n = 10, mean arterial pressure (MAP) = 183 + 18 (SD) mm Hg) and in control kidneys of unilateral nephrectomized rats (n = 14, MAP = 120 ± 14 mm Hg). Following saralasin infusion, no significant MAP change occurred in either group. Renal perfusion pressure of clamped kidneys (115 ± 13 mm Hg) was not different from MAP in controls. Hydrostatic pressure in glomerular capillaries in clamped kidneys was not different from that in controls (60.9 + 2.1 vs. 61.7 + 3.5 mm Hg). Early proximal flow rate, as a measure for single-nephron GFR, was decreased to 29.5 + 1.5 vs. 36.6 + 4.4 nl/min in controls (p < 0.01). Total renal resistance was increased by 102% in the hypertensive group, mainly due to the stenosis (75%) rather than the renal vasculature (27%). Due to a predominant increase of postglomerular vascular resistance, filtration fraction was increased in clamped kidneys (0.37 + 0.05 vs. 0.34 + 0.06, p < 0.001). Single nephron glomerular plasma flow was decreased to 158 + 23.5 vs. 209 + 45.1 nl/min in controls (p < 0.001). Efferent net ultrafiltration pressure did not differ significantly from zero in either group, i.e. filtration equilibrium was achieved. These results indicate an increased vascular resistance in clamped kidneys, which is caused by a preferential efferent vasocon-striction. This pattern of the vascular bed helps to prevent a further reduction of GFR despite a decrease of blood flo