Salt-sensitive hypertension in bradykinin B2 receptor knockout mice

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetylcholine / pharmacology
  • Animals
  • Bradykinin / pharmacology
  • Homeostasis
  • Hypertension / chemically induced*
  • Hypertension / genetics*
  • Hypertension / physiopathology
  • Kallikrein-Kinin System / physiology
  • Kidney / pathology
  • Mice
  • Mice, Knockout
  • Myocardium / pathology
  • Organ Size
  • Receptor, Bradykinin B2
  • Receptors, Bradykinin / drug effects
  • Receptors, Bradykinin / genetics*
  • Sodium Chloride / pharmacology*


  • Receptor, Bradykinin B2
  • Receptors, Bradykinin
  • Sodium Chloride
  • Acetylcholine
  • Bradykinin