Expression of KCNA10, a voltage-gated K channel, in glomerular endothelium and at the apical membrane of the renal proximal tubule

Potassium (K) channels regulate cell membrane po- tential and modulate a number of important cellular functions. KCNA10 is a cyclic nucleotide-gated, voltage-activated K channel that is detected in kidney, heart, and aorta by Northern blot and postulated to participate in renal K metabolism and to regulate vascular tone. The aim of this study was to establish the cellular and subcellular localization of KCNA10 in kidney and vascular tissues. An anti-KCNA10 polyclonal antibody was generated, and immunocytochemical studies were per- formed on rat kidney. KCNA10 protein was easily detectable at the apical membrane of rat proximal tubular cells, and a weaker signal was also evident in the glomerulus. In situ hybridization experiments confirmed the immunocytochemical studies and revealed KCNA10 expression in human proximal tubular cells, glomerular and vascular endothelial cells, and also in vascular smooth muscle cells. The data suggest that KCNA10 may facilitate proximal tubular sodium absorption by stabilizing cell membrane voltage. Furthermore, its presence in endothelial and vascular smooth muscle cells supports the notion that it also regulates vascular tone. Potassium (K) channels are membrane proteins that participate in many cellular processes primarily by regulating membrane potential. KCNA10 is a voltage-gated K (Kv) channel gene related to the Shaker superfamily (1), and its most distinguish- ing feature relates to the presence of a putative cyclic nucle- otide-binding (CNB) domain at the carboxy terminus. A few other K channels also contain CNB domains and may belong to new subclass of K channels with structural features common to