Proinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K+) channels induces changes in transepithelial transport of solutes and water in the kidney, since K+channels in tubule cells are indispensable for formation of membrane potential which serves as a driving force for the transepithelial transport. Altered K+channel activity may be involved in renal cell dysfunction during inflammation. Although little information was available regarding the effects of proinflammatory cytokines on renal K+channels, reports have emerged during the last decade. In human proximal tubule cells, interferon-γshowed a time-dependent biphasic effect on a 40 pS K+channel, that is, delayed suppression and acute stimulation, and interleukin-1βacutely suppressed the channel activity. Transforming growth factor-β1 activated KCa3.1 K+channel in immortalized human proximal tubule cells, which would be involved in the pathogenesis of renal fibrosis. This review discusses the effects of proinflammatory cytokines on renal K+channels and the causal relationship between the cytokine-induced changes in K+channel activity and renal dysfunction.
Electrophysiology and ultrastructure of cultured human proximal tubule cells