Korean J Physiol Pharmacol.
2000 Oct;4(5):385-391.
Alteration of 4-aminopyridine-sensitive, voltage-dependent K+-channel
in arterial smooth muscle cells of one-kidney, one-clip Goldblatt
hypertensive rats
- Affiliations
-
- 1Department of Physiology, College of Medicine, Konyang University,
26 Nae-dong, Nonsan, Chungnam, South Korea.
sehkim@kytis.konyang.ac.kr
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 +/- 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.