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KMID : 0811720000040050385
Korean Journal of Physiology & Pharmacology
2000 Volume.4 No. 5 p.385 ~ p.392
Alteration of 4-Aminopyridine-Sensitive, Voltage-Dependent K - Channel in Arterial Smooth Muscle Cells of One-Kidney, One-Clip Goldblatt Hypertensive Rats
Se-Hoon Kim/Hoe-Suk Kim
Se-Hoon Kim/Byeong-Hwa Jeon/Seok-Jong Chang
Abstract
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¡¾3.2mV) was reduced when compared to that of normotensive cell (?59.5¡¾2.8mV). Outward K+ current of hypertensive cell was significantly reduced when compared to normotensive cell. At 60 mV, the outward currents were 19.10¡¾1.91 and 14.06¡¾1.05 pA/pF in normotensive cell and hypertensive cell respectively. 4-AP-sensitive K+ current was also smaller in hypertensive cell (4.28¡¾0.38pA/pF) than in normotensive cell (7.65¡¾0.52pA/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.
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