Alteration of 4-Aminopyridine-Sensitive, Voltage-Dependent K<SUP>&#8290;</SUP>- Channel in Arterial Smooth Muscle Cells of One-Kidney, One-Clip Goldblatt Hypertensive Rats

Alteration of 4-Aminopyridine-Sensitive, Voltage-Dependent K<SUP>&#8290;</SUP>- Channel in Arterial Smooth Muscle Cells of One-Kidney, One-Clip Goldblatt Hypertensive Rats

<P> Using the patch-clamp technique, we investigated the alteration of 4-aminopyridine(4-AP)-sensitive, voltage-dependent K<SUP>&#8290; </SUP>channel (Kv) in the mesenteric arterial smooth muscle cell (MASMC) of renovascular hypertensive model, one-kidney one-clip Goldblatt hypertensive rat (GBH). To isolate K<SUB>V</SUB> 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 (&#8291;40.3&#8273;3.2 mV) was reduced when compared to that of normotensive cell (&#8291;59.5&#8273;2.8 mV). Outward K<SUP>&#8290;</SUP> current of hypertensive cell was significantly reduced when compared to normotensive cell. At 60 mV, the outward currents were 19.10&#8273;1.91 and 14.06&#8273;1.05 pA/pF in normotensive cell and hypertensive cell respectively. 4-AP-sensitive K<SUP>&#8290;</SUP> current was also smaller in hypertensive cell (4.28&#8273;0.38 pA/pF) than in normotensive cell (7.65&#8273;0.52 pA/pF). The values of half activation voltage (V<SUB>1/2</SUB>) and slope factor (<I>k1</I>) as well as the values of half inactivation voltage (V<SUB>1/2</SUB>) and slope factor (<I>k1</I>) were virtually similar between GBH and NTR. These results suggest that the decrease of 4-AP-sensitive K<SUP>&#8290;</SUP> current contributes to a depolarization of membrane potential, which leads to development of vascular tone in GBH.