Acute hypertension inhibits proximal tubule (PT) fluid reabsorption. The resultant increase in end proximal flow rate provides the error signal to mediate tubuloglomerular feedback (TGF) autoregulation of renal blood flow and glomerular filtration rate, and suppresses renal renin secretion. To test whether the suppression of the renin-angiotensin system during acute hypertension affects the magnitude of the inhibition of PT fluid and sodium reabsorption, plasma Ang II levels were clamped by infusion of the angiotensin converting enzyme (ACE) inhibitor captopril (12 µg/min), and Ang II after pretreatment with the bradykinin B₂ receptor blocker HOE-140 (100 µg/kg bolus). Since ACE also degrades bradykinin, HOE-140 was included to block effect of accumulating vasodilatory bradykinins during captopril infusion. HOE-140 increased the sensitivity of arterial blood pressure to Ang II: after captopril infusion without HOE-140, 20 ng/kg.min Ang II had no pressor effect, whereas with HOE-140 20 ng/kg.min Ang II increased blood pressure from 104 ± 4 to 140 ± 6 mmHg. Ang II infused at 2 ng/kg.min had no pressor effect after captopril and HOE-140 infusion ("Ang II clamp"). When blood pressure was acutely increased 50-60 mmHg by arterial constriction without Ang II clamp, urine output and endogenous lithium clearance increased 4.0-fold and 6.7-fold, respectively. With Ang II clamp, the effects of acute hypertension were reduced 50%: urine output and endogenous lithium clearance increased 2.0-fold and 3.0-fold, respectively. We conclude that HOE-140, an inhibitor of the B2 receptor, potentiates the sensitivity of arterial pressure to Ang II, and that clamping systemic Ang II levels during acute hypertension blunts the magnitude of the pressure diuretic response.