Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice

Roberta Maestri, Anna Franca Milia, Maria Bonaria Salis, Gallia Graiani, Costanza Lagrasta, Manuela Monica, Domenico Corradi, Costanza Emanueli, Paolo Madeddu

Research output: Contribution to journalArticle

Abstract

Experimental and clinical evidence suggests kinin involvement in adaptive myocardial growth. Kinins are growth-inhibitory to cardiomyocytes. Knockout of kinin B2 receptor (B2R) signaling causes dilated and failing cardiomyopathy in 129/J mice, and a 9-bp deletion polymorphism of human B2R is associated with reduced receptor expression and exaggerated left ventricular growth response to physical stress. We reasoned that genetic background and aging may significantly influence the impact of B2R mutation on cardiac phenotype. The theory was challenged in C57BL/6 mice, a strain that naturally differs from the 129/J strain, carrying 1 instead of 2 renin genes. C57BL/6 B2R knockouts (B2R-KO) showed higher blood pressure and heart rate levels (P

Original languageEnglish
Pages (from-to)1151-1155
Number of pages5
JournalHypertension
Volume41
Issue number5
DOIs
Publication statusPublished - May 1 2003

Keywords

  • Bradykinin
  • Cardiac function
  • Genes
  • Heart failure
  • Hypertension, essential

ASJC Scopus subject areas

  • Internal Medicine

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    Maestri, R., Milia, A. F., Salis, M. B., Graiani, G., Lagrasta, C., Monica, M., Corradi, D., Emanueli, C., & Madeddu, P. (2003). Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice. Hypertension, 41(5), 1151-1155. https://doi.org/10.1161/01.HYP.0000064180.55222.DF