Using the patch-clamp technique, we investigated the alteration of 4-aminopyridine(4-AP)-sensitive, voltage-dependent K⁢ channel (Kv) in the mesenteric arterial smooth muscle cell (MASMC) of renovascular hypertensive model, one-kidney one-clip Goldblatt hypertensive rat (GBH). To isolate KV current, internal pipette solution contained 5 mM ATP and 10 mM EGTA. Under these condition, MASMC was depolarized by 4-AP, but charybdotoxin did not affect membrane potential. Membrane potential of hypertensive cell (⁣40.3⁑3.2 mV) was reduced when compared to that of normotensive cell (⁣59.5⁑2.8 mV). Outward K⁢ current of hypertensive cell was significantly reduced when compared to normotensive cell. At 60 mV, the outward currents were 19.10⁑1.91 and 14.06⁑1.05 pA/pF in normotensive cell and hypertensive cell respectively. 4-AP-sensitive K⁢ current was also smaller in hypertensive cell (4.28⁑0.38 pA/pF) than in normotensive cell (7.65⁑0.52 pA/pF). The values of half activation voltage (V1/2) and slope factor (k1) as well as the values of half inactivation voltage (V1/2) and slope factor (k1) were virtually similar between GBH and NTR. These results suggest that the decrease of 4-AP-sensitive K⁢ current contributes to a depolarization of membrane potential, which leads to development of vascular tone in GBH.