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Cardiovascular Research 2000 48(2):194-210; doi:10.1016/S0008-6363(00)00184-X
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Kinin B1 receptors and the cardiovascular system: regulation of expression and function

Peter G. McLeana,b,*, Mauro Perrettib and Amrita Ahluwaliaa

aCenter for Clinical Pharmacology, Department of Medicine, The Rayne Institute, University College London, 5 University Street, London WC1E6JJ, UK
bDepartment of Biochemical Pharmacology, The William Harvey Research Institute, St. Bartholomew's and the Royal London School of Medicine and Dentistry, London EC1M6BQ, UK

* Corresponding author. Tel.: +44-207-679-6619; fax: +44-207-691-2838 p.mclean{at}ucl.ac.uk

Kinins are important peptide mediators of a diverse range of physiological and pathological functions of the cardiovascular system. The kinin peptides exert their effects by selective activation of two distinct G-protein coupled receptors termed B1 and B2. The principal kinin peptides involved in the acute regulation of cardiovascular function during normal physiology are bradykinin (BK) and Lys-BK which produce their effects via activation of B2 receptors. The B1 receptor is activated by the des-Arg9kinin metabolites namely des-Arg9BK and Lys-des-Arg9BK, the synthesis of which are increased during inflammation. The B1 receptor, which is not constitutively expressed, is induced in various pathologies relating to inflammation. Recent investigations into the molecular mechanisms of B1 receptor induction and their distribution and function in the cardiovascular system have shown that following an inflammatory stimulus the B1 receptor is induced and may play an important role in modulation of cardiovascular function. This review summarises recent studies on B1 receptor expression and function in the cardiovascular system and discusses the role of these receptors in regulation of circulatory homeostasis and their potential as therapeutic targets.

KEYWORDS G-proteins; Infection/inflammation; Receptors; Signal transduction


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