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

59 Citations (Scopus)

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

Fingerprint

Kinins
Cardiomegaly
Knockout Mice
Growth
129 Strain Mouse
Dilated Cardiomyopathy
Inbred C57BL Mouse
Renin
Cardiac Myocytes
Heart Rate
Hypertension
Phenotype
Mutation
Genes

Keywords

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

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Maestri, R., Milia, A. F., Salis, M. B., Graiani, G., Lagrasta, C., Monica, M., ... 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

Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice. / Maestri, Roberta; Milia, Anna Franca; Salis, Maria Bonaria; Graiani, Gallia; Lagrasta, Costanza; Monica, Manuela; Corradi, Domenico; Emanueli, Costanza; Madeddu, Paolo.

In: Hypertension, Vol. 41, No. 5, 01.05.2003, p. 1151-1155.

Research output: Contribution to journalArticle

Maestri, R, Milia, AF, Salis, MB, 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, vol. 41, no. 5, pp. 1151-1155. https://doi.org/10.1161/01.HYP.0000064180.55222.DF
Maestri R, Milia AF, Salis MB, Graiani G, Lagrasta C, Monica M et al. Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice. Hypertension. 2003 May 1;41(5):1151-1155. https://doi.org/10.1161/01.HYP.0000064180.55222.DF
Maestri, Roberta ; Milia, Anna Franca ; Salis, Maria Bonaria ; Graiani, Gallia ; Lagrasta, Costanza ; Monica, Manuela ; Corradi, Domenico ; Emanueli, Costanza ; Madeddu, Paolo. / Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice. In: Hypertension. 2003 ; Vol. 41, No. 5. pp. 1151-1155.
@article{c4d161c8814e41c3b3076b83fbc2c19d,
title = "Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice",
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",
keywords = "Bradykinin, Cardiac function, Genes, Heart failure, Hypertension, essential",
author = "Roberta Maestri and Milia, {Anna Franca} and Salis, {Maria Bonaria} and Gallia Graiani and Costanza Lagrasta and Manuela Monica and Domenico Corradi and Costanza Emanueli and Paolo Madeddu",
year = "2003",
month = "5",
day = "1",
doi = "10.1161/01.HYP.0000064180.55222.DF",
language = "English",
volume = "41",
pages = "1151--1155",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice

AU - Maestri, Roberta

AU - Milia, Anna Franca

AU - Salis, Maria Bonaria

AU - Graiani, Gallia

AU - Lagrasta, Costanza

AU - Monica, Manuela

AU - Corradi, Domenico

AU - Emanueli, Costanza

AU - Madeddu, Paolo

PY - 2003/5/1

Y1 - 2003/5/1

N2 - 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

AB - 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

KW - Bradykinin

KW - Cardiac function

KW - Genes

KW - Heart failure

KW - Hypertension, essential

UR - http://www.scopus.com/inward/record.url?scp=0037657981&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037657981&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.0000064180.55222.DF

DO - 10.1161/01.HYP.0000064180.55222.DF

M3 - Article

C2 - 12654715

AN - SCOPUS:0037657981

VL - 41

SP - 1151

EP - 1155

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 5

ER -