抄録
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.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 589-596 |
| ページ数 | 8 |
| ジャーナル | Hypertension Research |
| 巻 | 25 |
| 発行部数 | 4 |
| DOI | |
| 出版物ステータス | 出版済み - 1 1 2002 |
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All Science Journal Classification (ASJC) codes
- Internal Medicine
- Physiology
- Cardiology and Cardiovascular Medicine
これを引用
Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats. / Sadanaga, Tsuneaki; Ohya, Yusuke; Ohtsubo, Toshio; Goto, Kenichi; Fujii, Koji; Abe, Isao.
：: Hypertension Research, 巻 25, 番号 4, 01.01.2002, p. 589-596.研究成果: ジャーナルへの寄稿 › 記事
}
TY - JOUR
T1 - Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats
AU - Sadanaga, Tsuneaki
AU - Ohya, Yusuke
AU - Ohtsubo, Toshio
AU - Goto, Kenichi
AU - Fujii, Koji
AU - Abe, Isao
PY - 2002/1/1
Y1 - 2002/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0035993033&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035993033&partnerID=8YFLogxK
U2 - 10.1291/hypres.25.589
DO - 10.1291/hypres.25.589
M3 - Article
C2 - 12358146
AN - SCOPUS:0035993033
VL - 25
SP - 589
EP - 596
JO - Hypertension Research
JF - Hypertension Research
SN - 0916-9636
IS - 4
ER -