PMID- 12358146
OWN - NLM
STAT- MEDLINE
DCOM- 20030318
LR  - 20191025
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 25
IP  - 4
DP  - 2002 Jul
TI  - Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from 
      hypertensive rats.
PG  - 589-96
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.
FAU - Sadanaga, Tsuneaki
AU  - Sadanaga T
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Ohya, Yusuke
AU  - Ohya Y
FAU - Ohtsubo, Toshio
AU  - Ohtsubo T
FAU - Goto, Kenichi
AU  - Goto K
FAU - Fujii, Koji
AU  - Fujii K
FAU - Abe, Isao
AU  - Abe I
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (Drug Combinations)
RN  - 0 (Kcna5 protein, rat)
RN  - 0 (Kv1.5 Potassium Channel)
RN  - 0 (Potassium Channel Blockers)
RN  - 0 (Potassium Channels)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 115422-61-2 (Charybdotoxin)
RN  - 24345-16-2 (Apamin)
RN  - BH3B64OKL9 (4-Aminopyridine)
SB  - IM
MH  - 4-Aminopyridine/*pharmacology
MH  - Animals
MH  - Aorta
MH  - Apamin/pharmacology
MH  - Charybdotoxin/pharmacology
MH  - Drug Combinations
MH  - Endothelium, Vascular/*metabolism/pathology/physiopathology
MH  - Genetic Predisposition to Disease
MH  - Hypertension/*metabolism/physiopathology
MH  - Kv1.5 Potassium Channel
MH  - Male
MH  - Membrane Potentials/drug effects
MH  - Potassium Channel Blockers/*pharmacology
MH  - Potassium Channels/drug effects/metabolism
MH  - Potassium Channels, Voltage-Gated/*drug effects/*metabolism
MH  - Rats
MH  - Rats, Inbred SHR/genetics
MH  - Rats, Inbred WKY
MH  - Stroke/genetics
EDAT- 2002/10/03 04:00
MHDA- 2003/03/19 04:00
CRDT- 2002/10/03 04:00
PHST- 2002/10/03 04:00 [pubmed]
PHST- 2003/03/19 04:00 [medline]
PHST- 2002/10/03 04:00 [entrez]
AID - 10.1291/hypres.25.589 [doi]
PST - ppublish
SO  - Hypertens Res. 2002 Jul;25(4):589-96. doi: 10.1291/hypres.25.589.