The kallikrein-kinin system regulates water and sodium excretion and thus plays a role in blood pressure (BP) homeostasis. We tested the hypothesis that mice lacking the gene encoding for the bradykinin B₂receptor (B₂-KO) have a greater hypertensive response to chronic high Na⁺intake (salt sensitivity) compared to controls. We also obtained dose-response curves for different vasoactive substances in both groups. The hypertensive effect of high Na⁺intake was almost doubled in B₂-KO mice compared to controls. A high-Na⁺diet increased heart and kidney weight in B₂-KO, but not in controls, suggesting an increased afterload in B₂-KO mice. The BP response to bradykinin was completely abolished in B₂-KO, but that to acetylcholine was conserved. The hypertensive response to angiotensin II was not exaggerated in B₂-KO mice. This study describes a new salt-sensitive animal model and suggests that in mice kinins play a role in preventing salt-sensitive hypertension.