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Hypertension. 2001;37:1473-1479

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(Hypertension. 2001;37:1473.)
© 2001 American Heart Association, Inc.


Scientific Contributions

Normal Blood Pressure and Renal Function in Mice Lacking the Bradykinin B2 Receptor

Anna Franca Milia; Volkmar Gross; Ralph Plehm; Jose A. De Silva, Jr; Michael Bader; Friedrich C. Luft

From the Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine (A.F.M., V.G., R.P., J.A.D.S., M.B., F.C.L.), Medical Faculty of the Charité, Humboldt University of Berlin, Germany; and the National Institute of Biostructures and Biosystems (A.F.M.), Osilo, Italy.

Correspondence to Dr Friedrich C. Luft, Franz Volhard Clinic, Wiltberg Strasse 50, 13122 Berlin, Germany. E-mail luft{at}fvk-berlin.de

Abstract—Telemetric blood pressure determinations, heart rate measurements, and pressure-natriuresis-diuresis experiments were used to characterize cardiovascular and renal function in bradykinin B2 receptor knockout mice fed mouse chow containing 0.25% NaCl or mouse chow containing 4% NaCl. In B2 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 B1 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 B2 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 B2 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 B2 receptor function was verified in B2 receptor knockout mice with bradykinin infusion. These data suggest that the absence of B2 receptor function does not necessarily make B2 receptor knockout mice hypertensive or induce salt sensitivity. Presumably, differences in the genetic background or an adaptation to the loss of B2 receptor function may account for these results, in contrast with earlier reports involving B2 receptor knockout mice. We hold the latter possibility to be more likely and to be a fruitful possibility for future research.


Key Words: bradykinin • mice • natriuresis • kidney • sodium, dietary




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