Alfie M E, Yang X P, Hess F, Carretero O A
Department of Medicine and Heart, Henry Ford Hospital, Detroit, Michigan 48202, USA.
Biochem Biophys Res Commun. 1996 Jul 25;224(3):625-30. doi: 10.1006/bbrc.1996.1076.
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 B2 receptor (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.
激肽释放酶-激肽系统调节水和钠的排泄，因此在血压（BP）稳态中发挥作用。我们检验了这样一个假设：与对照组相比，缺乏缓激肽B2受体编码基因的小鼠（B2-KO）对慢性高钠摄入（盐敏感性）有更大的高血压反应。我们还获得了两组不同血管活性物质的剂量反应曲线。与对照组相比，B2-KO小鼠高钠摄入的高血压效应几乎翻倍。高钠饮食增加了B2-KO小鼠的心脏和肾脏重量，但对照组没有，这表明B2-KO小鼠的后负荷增加。B2-KO小鼠对缓激肽的血压反应完全消失，但对乙酰胆碱的反应保留。B2-KO小鼠对血管紧张素II的高血压反应没有增强。本研究描述了一种新的盐敏感动物模型，并表明在小鼠中激肽在预防盐敏感性高血压中发挥作用。
