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J. Pharmacol. Exp. Ther. · Sep 2005
Endogenous aminopeptidase N decreases the potency of peptide agonists and antagonists of the kinin B1 receptors in the rabbit aorta.
- Jean-Philippe Fortin, Lajos Gera, Johanne Bouthillier, John M Stewart, Albert Adam, and François Marceau.
- Centre de Recherche en Rhumatologie et Immunologie, Centre Hospitalier Universitaire de Québec, Canada.
- J. Pharmacol. Exp. Ther. 2005 Sep 1;314(3):1169-76.
AbstractThe B(1) receptor for kinins is selectively stimulated by bradykinin-related fragments lacking the C-terminal arginine, des-arginine(9)-bradykinin (des-Arg(9)-BK), and Lys-des-Arg(9)-BK. The latter peptide is the optimal agonist at the human and rabbit receptor. The B(1) receptor is inducible as a function of inflammatory conditions in the vasculature. We studied the effect of endogenously expressed peptidases on the potency of ligands of this receptor in an established bioassay, the rabbit aorta contractility. The potency measured for agonists (EC(50)) or antagonists (pA(2) scale) in this assay was compared with the affinity of each agent determined using [(3)H]Lys-des-Arg(9)-BK binding competition in cultured aortic smooth muscle cells and with the competition K(i) for the hydrolysis of the aminopeptidase chromogenic substrate L-Ala-p-nitroanilide by smooth muscle cell membranes. The contractile potency of the agonist Lys-des-Arg(9)-BK is decreased by in situ metabolism, and aminopeptidase N mediates most of the distortion (inhibited by amastatin but not efficiently by puromycin). At the other end of the spectrum, the fully protected agonist Sar-[D-Phe(8)]des-Arg(9)-BK is not significantly potentiated by peptidase inhibitors. A similar distortion of apparent potency was observed for some peptide antagonists used in the contractility assay, B-10350 (Lys-Lys-[Hyp(3), Igl(5), d-Tic(7), CpG(8)]des-Arg(9)-BK) and Lys-[Leu(8)]des-Arg(9)-BK being intensely potentiated by amastatin treatment and effective L-Ala-p-nitroanilide competitors. N-Protected peptide antagonists or a nonpeptide antagonist of the B(1) receptor were not potentiated by amastatin. The coexpression of aminopeptidase N and the kinin B(1) receptor in rabbit arterial tissue is of interest for the inactivation of the high-affinity agonist Lys-des-Arg(9)-BK and for the design of hydrosoluble antagonist drugs.
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