Endothelial cell function is altered in hypertension. The present study was performed to evaluate the alterations in K+ channels in endothelial cells from hypertensive rats. Currents and membrane potentials were recorded in endothelial cells freshly dissociated from the aorta of stroke-prone spontaneously hypertensive rats (SHR-SP) and Wistar-Kyoto rats (WKY). Ca2+-dependent K+ channel blockers, charybdotoxin and apamin, a voltage-dependent K+ channel blocker, 4-aminopyridine, and a non-selective K+ channel blocker, tetrabutylammonium, were used to characterize K+ currents. Depolarizing command steps evoked delayed K+ outward currents in cells from both strains. The current density of 4-aminopyridine sensitive K+ currents was significantly smaller in SHR-SP than in WKY (1.5 +/- 0.4 vs. 4.9 +/- 0.6 pA/pF, at 36 mV, n = 13, p < 0.01), whereas that of other K+ current components did not differ between strains. The resting membrane potential of cells was significantly less negative in SHR-SP than in WKY (-25.0 +/- 1.7, n = 54 vs. -33.5 +/- 1.4 mV, n = 50, p < 0.01). Depolarization by 4-aminopyridine, but not that by charybdotoxin+apamin, abolished the difference in membrane potentials between SHR-SP and WKY (n=7-10 in each strain). Immunostaining of endothelial cells by anti-Kv1.5 antibody was decreased in SHR-SP compared to WKY. In summary, the 4-aminopyridine sensitive K+ currents in aortic endothelial cells were decreased in SHR-SP, which could contribute to the membrane depolarization. Decreased expression of Kv1.5 in SHR-SP might be associated with this alteration.