Abstract:
:With respect to functional aspects, the kallikrein-kinin-system can be divided into a plasma kallikrein-kinin-system and a tissue kallikrein-kinin-system. At least four functional kinin peptides act via two different G-protein-coupled receptors, an inducible B1-receptor and a constitutively expressed B2-receptor. B1R and B2R couple to G(q/11) and lead via phospholipase C to Ca2+ mobilization. In humans both, bradykinin and kallidin are agonists on the B2-receptor. In contrast, bradykinin is believed to be the only kinin acting on the B2R in rats and mice. However, recently we have isolated a kallidin-like-peptide from plasma and urine of rats. Until now the kinin ligand-receptor interactions were mainly characterized in binding studies. However, receptor affinity does not inevitably correspond with the intrinsic activity of an agonist. The aim of the present study was to investigate intracellular calcium mobilization to quantify mouse, rat and human B1- and B2-receptor activation by bradykinin, kallidin, des-Arg9-bradykinin, des-Arg10-kallidin, and of the two novel rat kinins, kallidin-like-peptide and des-Arg10-kallidin-like-peptide. In cells stably expressing the human, rat, and mouse B2-receptor, respectively, bradykinin, kallidin, and kallidin-like-peptide were nearly equipotent (EC50, 10(-12)M) at eliciting Ca2+-transients. Their des-Arg-derivatives were 10(3)-fold less potent. In cells expressing B1-receptor the des-Arg derivatives elicited Ca2+-signals at an EC50 in the order of 10(-9)M. Major differences between these peptides could not be observed. Bradykinin, kallidin, and kallidin-like-peptide caused a Ca2+-signal at substantially higher concentrations in the order of 10(-7)M. The data show that des-Arg9-bradykinin, des-Arg10-kallidin, and des-Arg10-kallidin-like-peptide are equipotent agonists at the B1-receptor. Bradykinin, kallidin and kallidin-like-peptide are equipotent agonists at the B2-receptor.
journal_name
Int Immunopharmacoljournal_title
International immunopharmacologyauthors
Zubakova R,Gille A,Faussner A,Hilgenfeldt Udoi
10.1016/j.intimp.2007.10.001subject
Has Abstractpub_date
2008-02-01 00:00:00pages
276-81issue
2eissn
1567-5769issn
1878-1705pii
S1567-5769(07)00311-6journal_volume
8pub_type
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