Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.