['To elucidate the modulation of the chemerin/ChemR23 axis by iptakalim-induced opening of K(ATP) channels and to determine the role of the chemerin/ChemR23 axis in the iptakalim-mediated endothelial protection.', 'Cultured rat aortic endothelial cells (RAECs) were used. Chemerin secretion and ChemR23 protein expression were investigated using Western blot analysis. The gene expression level of ChemR23 was examined with RT-PCR. In addition, the release of nitric oxide (NO) was measured with a nitric oxide assay.', 'Homocysteine, uric acid, high glucose, or oxidized low-density lipoprotein (ox-LDL) down-regulated the chemerin secretion and ChemR23 gene/protein expression in RAECs as a function of concentration and time, which was reversed by pretreatment with iptakalim (1-10 μmol/L). Moreover, these effects of iptakalim were abolished in the presence of the K(ATP) channel antagonist glibenclamide (1 μmol/L). Both iptakalim and recombinant chemerin restored the impaired NO production in RAECs induced by uric acid, and the effects were abolished by anti-ChemR23 antibodies.'] Is chemerin/ChemR23 signaling axis involved in the endothelial protection by K ( ATP ) channel opener iptakalim?