抄録
Interleukin-1β (IL-1β) influences cell injury in various organs during inflammatory diseases. Although some investigators reported that changes in K+ channel activity were involved in the renal tubular cell injury induced by endotoxemia or ischemia, little information is available regarding effects of cytokines on activity of renal K+ channels. In this study, we investigated the effects of IL-1β on activity of an inwardly rectifying K+ channel (Gi: 40 pS, Go: 7 pS) in cultured human proximal tubule cells, using the cell-attached mode of patch-clamp technique. IL-1β (15 pg/ml) reversibly suppressed the K+ channel activity in a few minutes after its addition to the bath. This acute suppressive effect was blocked by IL-1 receptor antagonist (20 ng/ml). 8Br-cAMP (100 μM) or 8Br-cGMP (100 μM) did not stimulate channel activity in the presence of the suppressive effect of IL-1β. A PKC inhibitor, GF109203X (500 nM), reactivated the channel suppressed by IL-1β. Furthermore, pretreatment of cells with GF109203X prevented the suppression of channel activity by IL-1β. These results suggested that IL-1β acutely suppressed activity of the 40 pS K+ channel in cultured human proximal tubule cells by impairing the PKA/PKG pathways and activating PKC-mediated phosphorylation processes. [J Physiol Sci. 2008;58 Suppl:S205]
