Increased expression of bradykinin type-1 receptors in endothelium of intramyocardial coronary vessels in human failing hearts

In experimental animals, bradykinin type-1 receptors (BK-1Rs) are induced during inflammation and ischemia, and, by exerting either cardioprotective or cardiotoxic effects, they may contribute to the pathogenesis of heart failure. Nothing is known about the expression of BK-1Rs in human heart failur...

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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 57; no. 5; pp. H2317 - H2322
Main Authors LIESMAA, Inka, KUOPPALA, Antti, SHIOTA, Naotaka, KOKKONEN, Jorma O, KOSTNER, Karam, MÄYRÄNPÄÄ, Mikko, KOVANEN, Petri T, LINDSTEDT, Ken A
Format Journal Article
LanguageEnglish
Published Bethesda, MD American Physiological Society 01.05.2005
Subjects
Biological and medical sciences
Coronary vessels
Fundamental and applied biological sciences. Psychology
Gene expression
Heart failure
Human subjects
Vertebrates: cardiovascular system
Heart
Human
Heart failure
cardiotoxic
Peptide hormone
Cytokine
Cardiovascular disease
Inflammation
Coronary vessel
Neuropeptide
Endothelium
Vertebrata
Mammalia
Heart disease
Bradykinin
Circulatory system
Intramyocardial
end-stage heart failure
Biological receptor
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Summary:In experimental animals, bradykinin type-1 receptors (BK-1Rs) are induced during inflammation and ischemia, and, by exerting either cardioprotective or cardiotoxic effects, they may contribute to the pathogenesis of heart failure. Nothing is known about the expression of BK-1Rs in human heart failure. Human heart tissue was obtained from excised hearts of patients undergoing cardiac transplantation (n = 13), due to idiopathic dilated cardiomyopathy (IDC; n = 7) or to coronary heart disease (CHD; n = 6), and from normal hearts (n = 6). The expression of BK-1Rs was analyzed by means of competitive RT-PCR, Western blot analysis, and immunohistochemistry. Expression of BK-1R mRNA was increased in both IDC (2.8-fold) and CHD (2.1-fold) hearts compared with normal hearts. The observed changes were verified at the protein level. Expression of BK-1Rs in failing hearts localized to the endothelium of intramyocardial coronary vessels and correlated with an increased expression of TNF-{alpha} in the vessel wall. Treatment of human coronary artery endothelial cells with TNF-{alpha} increases their BK-1R expression. These novel results show that BK-1Rs are induced in the endothelium of intramyocardial coronary vessels in failing human hearts and so may participate in the pathogenesis of heart failure. [PUBLICATION ABSTRACT]
ISSN:0363-6135
1522-1539