Andronic, J.J.AndronicBobak, N.N.BobakBittner, S.S.BittnerEhling, P.P.EhlingKleinschnitz, C.C.KleinschnitzHerrmann, A.M.A.M.HerrmannZimmermann, H.H.ZimmermannSauer, M.M.SauerWiendl, H.H.WiendlBudde, T.T.BuddeMeuth, S.G.S.G.MeuthSukhorukov, V.L.V.L.Sukhorukov2022-03-042022-03-042013https://publica.fraunhofer.de/handle/publica/23221910.1016/j.bbamem.2012.09.028Many functions of T lymphocytes are closely related to cell volume homeostasis and regulation, which utilize a complex network of membrane channels for anions and cations. Among the various potassium channels, the voltage-gated K(v)1.3 is well known to contribute greatly to the osmoregulation and particularly to the potassium release during the regulatory volume decrease (RVD) of T cells faced with hypotonic environment. Here we address a putative role of the newly identified two-pore domain (K-2P) channels in the RVD of human CD4(+) T lymphocytes, using a series of potent well known channel blockers. In the present study, the pharmacological profiles of RVD inhibition revealed K(2P)5.1 and K(2P)18.1 as the most important K-2P channels involved in the RVD of both naive and stimulated T cells. The impact of chemical inhibition of K(2P)5.1 and K(2P)18.1 on the RVD was comparable to that of K(v)1.3. K(2P)9.1 also notably contributed to the RVD of T cells but the extent of this contribution and its dependence on the activation status could not be unambiguously resolved. In summary, our data provide first evidence that the RVD-related potassium efflux from human T lymphocytes relies on K-2P channels.en610571journal article