Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats

Tsuneaki Sadanaga, Yusuke Ohya, Toshio Ohtsubo, Kenichi Goto, Koji Fujii, Isao Abe

研究成果: ジャーナルへの寄稿記事

15 引用 (Scopus)

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
25
発行部数4
DOI
出版物ステータス出版済み - 1 1 2002

Fingerprint

4-Aminopyridine
Inbred WKY Rats
Endothelial Cells
Membrane Potentials
Charybdotoxin
Apamin
Inbred SHR Rats
Aorta
Stroke
Hypertension
Membranes

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

Sadanaga, Tsuneaki ; Ohya, Yusuke ; Ohtsubo, Toshio ; Goto, Kenichi ; Fujii, Koji ; Abe, Isao. / Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats. :: Hypertension Research. 2002 ; 巻 25, 番号 4. pp. 589-596.
@article{93dc20aebf864f209b8557729f37efb6,
title = "Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats",
abstract = "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.",
author = "Tsuneaki Sadanaga and Yusuke Ohya and Toshio Ohtsubo and Kenichi Goto and Koji Fujii and Isao Abe",
year = "2002",
month = "1",
day = "1",
doi = "10.1291/hypres.25.589",
language = "English",
volume = "25",
pages = "589--596",
journal = "Hypertension Research",
issn = "0916-9636",
publisher = "Nature Publishing Group",
number = "4",

}

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 -