Experiments were performed in anesthetized rats to examine the effect of an intravenous infusion of norepinephrine or vasopressin on the tubuloglomerular feedback (TGF) response of stop flow pressure (P_SF). During infusion of norepinephrine at an average rate of 107.5 ng/kg mm, mean femoral arterial pressure (MAP) increased from 102.1±3.55 to 113.7±3.44 mm Hg and P_SF-max increased from 7.45±1.13 to 9.95±1.19 mm Hg. When MAP was returned to control by a suprarenal aortic clamp P_SF-max was 5.64±1.09 mm Hg (NS vs. control). Similarly, at an infusion rate of 226.5 ng/kg mm P_SF-max was not significantly different from control (6.79±1.61 mm Hg). V_1/2, the half-maximum flow rate, was not altered by norepinephrine whether MAP increased or was kept constant. Infusion of vasopressin at the pressor dose of 13.0 mU/kg mm increased MAP by about 25 mm Hg and raised P_SF-max from 6.56±0.84 to 14.45±1.54 mm Hg. However, when MAP was returned to normal P_SF-max was 5.41±0.75 mm Hg (NS). Our data show that in contrast to angiotensin II, norepinephrine and vasopressin do not augment TGF responses when a rise in MAP is prevented. Angiotensin II appears to play a specific role in altering the sensitivity of the TOF mechanism.