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Salt-Sensitive Hypertension in Bradykinin B2Receptor Knockout Mice

https://doi.org/10.1006/bbrc.1996.1076Get rights and content

Abstract

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.

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Abbreviations: K-K, kallikrein-kinin; ACE, angiotensin-converting enzyme; BP, blood pressure; Ang II, angiotensin II; BK, bradykinin; B2-KO, bradykinin B2receptor knockout mouse; Ach, acetylcholine.

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