Abstract —Telemetric blood pressure determinations, heart rate measurements, and pressure-natriuresis-diuresis experiments were used to characterize cardiovascular and renal function in bradykinin B ₂ receptor knockout mice fed mouse chow containing 0.25% NaCl or mouse chow containing 4% NaCl. In B ₂ receptor knockout mice fed usual mouse chow, the mean arterial blood pressure leveled between 108±1 and 110±3 mm Hg, and the heart rate leveled between 520±26 and 525±29 bpm, values that were not different from those measured in B ₁ receptor knockout mice or 129Sv/J control mice. Increasing dietary salt intake did not affect mean arterial blood pressure and heart rate. Accordingly, pressure-natriuresis curves, pressure-diuresis curves, renal blood flow, and glomerular filtration rate were not different between B ₂ receptor knockout and 129Sv/J mice. Increasing dietary salt intake to 4% increased renal blood flow to levels between 8.41 and 9.50 mL/min per gram kidney wet weight in 129Sv/J mice, whereas in B ₂ receptor–deficient mice, renal blood flow was not affected and ranged between 6.85 and 7.88 mL/min per gram kidney wet weight. Other renal function parameters were not affected. Absence of B ₂ receptor function was verified in B ₂ receptor knockout mice with bradykinin infusion. These data suggest that the absence of B ₂ receptor function does not necessarily make B ₂ receptor knockout mice hypertensive or induce salt sensitivity. Presumably, differences in the genetic background or an adaptation to the loss of B ₂ receptor function may account for these results, in contrast with earlier reports involving B ₂ receptor knockout mice. We hold the latter possibility to be more likely and to be a fruitful possibility for future research.