Suporn SukrittanonWattana B. WatanapaKatesirin RuamyodMahidol University2018-11-092018-11-092014-10-12Life Sciences. Vol.115, No.1 (2014), 15-2118790631002432052-s2.0-84908027562https://repository.li.mahidol.ac.th/handle/20.500.14594/33219© 2014 Elsevier Inc. All rights reserved. Main methods: Ionic currents of cultured HCAECs were studied using whole-cell patch clamp technique. Aims: Ginsenosides, active components in ginseng, have been shown to increase nitric oxide (NO) production in aortic endothelial cells. This effect was reversed by tetraethylammonium (TEA) inhibition of endothelial Ca2+-activated K+(KCa) channels. The objectives of this study, therefore, were to test 1) whether vasorelaxing ginsenoside Re could affect KCacurrent, an important regulator of NO production, in human coronary artery endothelial cells (HCAECs); and 2) whether small-conductance KCa(SKCa) channel was the channel subtype involved.Key findings: Ginsenoside Re dose-dependently increased endothelial outward currents, with an EC50of 408.90±1.59 nM, and a maximumincrease of 36.20± 5.62% (mean±SEM; p <0.05). Apamin, an SKCachannel inhibitor, could block this effect, while La3+, a nonselective cation channel (NSC) blocker, could not.When NSC channel, inward-rectifier K+channel, intermediate-, and large-conductance KCachannels were simultaneously blocked, ginsenoside Re could still increase outward currents significantly (35.49± 4.22%; p b 0.05); this effect was again abolished by apamin. Repeating the experiments when Cl? channel was additionally blocked gave similar results. Finally, we demonstrated that ginsenoside Re could hyperpolarize HCAECs; this effect was reversed by apamin. These data clearly indicate that ginsenoside Re increased HCAEC outward current via SKCachannel activation, and NSC channel was not involved.Significance: This is the first report to demonstrate that ginsenoside Re could increase SKCachannel activity in HCAECs. This can be a mechanism mediating ginseng's beneficial actions on coronary vessels.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicinePharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1016/j.lfs.2014.09.007