Normal blood pressure and renal function in mice lacking the bradykinin B(2) receptor.

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.