Ca2+-activated K+ channels (KCa) in endothelial cells and their response to some pharmacological agents are well known. However, the regulative function of these channels on transmembrane potential under ischemic conditions is still obscure. Therefore, we examine the effects of some ischemic factors on KCa channels in cultured human umbilical vein endothelial cells (HUVEC) by means of the patch-clamp technique. In whole-cell recordings (test potentials: -60mV to±100mV) the perfusion with an artificial (“ischemic”) Tyrode solution (pH=6.8; pO2=45mmHg, glucose-free) of HUVEC caused a significant increase of an outward current in the voltage range of +40mV to±100mV (P<0.05; n=15; Fig. 1: I/V-relationship, mean values; Fig. 2: sample of recordings). These currents were completely blOCked by extracellular tetraethylammonium (TEA: 0.5mM). whereas glibenclamide (10μM) had no effect. In cell-attached patches (140mM K+ pipette solution) KCa channels were characterized by their typical voltage dependence, their block by TEA and a single-channel slope conduction of 215 pS (±5.17 pS; n<10). Superfusion of HUVEC with the artificial solution caused a significant increase in the open-state probability NPo (N: channels in the patch) of KCa channels from 0.0141±0.0056 to 0.0377±0.0119 at +80mV (p<0.05: n=6) and 0.0645±0.0221 to 0.1599±0.0485 at+100mV (p<0.05; n=7)(Fig. 3: sample of KCa recordings). Single channel conductance was not found to be changed. We conclude that the KCa channel in endothelial cells isinfluenced by basic ischemic factors and may, under pathophysiological conditions, be of importance in regulating Ca2+-entry and stimulation-secretion coupling by modulating membrane potential.