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- Marie-Thérèse Bawolak and François Marceau.
- Centre de recherche en Rhumatologie et Immunologie, Centre Hospitalier Universitaire de Québec, 2705 Laurier Blvd., Québec (Québec), Canada G1V 4G2.
- Regul. Pept. 2007 May 3;140(3):125-30.
AbstractZaltoprofen is a nonsteroidal antiinflammatory drug that has been proposed to inhibit with some selectivity the nociception mediated by the bradykinin (BK) B(2) receptor. In order to test the predictive power of this claim, we applied the drug to vascular smooth muscle assays previously found useful to characterize B(2) receptor antagonists (contractility, human isolated umbilical vein) or B(1) receptor antagonists (contraction, rabbit aorta; relaxation, rabbit mesenteric artery). Zaltoprofen (up to 30 microM) failed to antagonize BK or des-Arg(9)-BK-induced contraction in the umbilical vein and aorta, respectively. The drug (1 microM) abated des-Arg(9)-BK-induced, prostaglandin-mediated relaxation of the precontracted mesenteric artery, consistent with its known activity as a cyclooxygenase (COX) inhibitor. However, zaltoprofen (10 microM) did not inhibit kinin-stimulated phospholipase A(2) activity in HEK 293 cells expressing recombinant forms of the rabbit B(1) or B(2) receptors. Nonpeptide antagonists of either receptor subtype were active in this respect. The results do not support that zaltoprofen, a COX inhibitor, antagonizes kinin receptors or influences their signaling with selectivity in the tested systems.
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