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Salt-sensitive hypertension in bradykinin B2 receptor knockout mice.

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 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.
AuthorsM E Alfie, X P Yang, F Hess, O A Carretero
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 224 Issue 3 Pg. 625-30 (Jul 25 1996) ISSN: 0006-291X [Print] United States
PMID8713099 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Receptor, Bradykinin B2
  • Receptors, Bradykinin
  • Sodium Chloride
  • Acetylcholine
  • Bradykinin
Topics
  • Acetylcholine (pharmacology)
  • Animals
  • Bradykinin (pharmacology)
  • Homeostasis
  • Hypertension (chemically induced, genetics, physiopathology)
  • Kallikrein-Kinin System (physiology)
  • Kidney (pathology)
  • Mice
  • Mice, Knockout
  • Myocardium (pathology)
  • Organ Size
  • Receptor, Bradykinin B2
  • Receptors, Bradykinin (drug effects, genetics)
  • Sodium Chloride (pharmacology)

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