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Characteristics and a functional implication of Ca2+-activated K+ current in mouse aortic endothelial cells

Title
Characteristics and a functional implication of Ca2+-activated K+ current in mouse aortic endothelial cells
Authors
Ahn S.C.Seol G.H.Kim J.A.Suh S.H.
Ewha Authors
서석효
SCOPUS Author ID
서석효scopus
Issue Date
2004
Journal Title
Pflugers Archiv European Journal of Physiology
ISSN
0031-6768JCR Link
Citation
vol. 447, no. 4, pp. 426 - 435
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
We employed the patch-clamp technique to investigate a Ca 2+-activated K+ (KCa) current in cultured mouse aortic endothelial cells (MAECs). In the whole-cell mode, an increase in cytosolic [Ca2+] ([Ca2+]i) to 2 μM activated an outwards current. The [K+]o-dependent change of the reversal potentials agreed well with the predicted Nernstian relation, suggesting that it was a KCa current. The Hill coefficient (4) and EC50 (740 nM) were obtained from the current/[Ca2+] i relationship. Iberiotoxin (50 nM) or apamin (200 nM) failed to inhibit the current, whereas TEA (10 mM) suppressed the current to 73.6 ±1.6% of control (n=9). The intermediate-conductance, Ca 2+-activated K+ (IKCa) channel blockers charybdotoxin (50 nM), clotrimazole (10 μM) and econazole (10 μM) inhibited the KCa current to 10.5±1.3% (n=6), 16.6±3. 1% (n=6), and 19.3±2.5% (n=5) of control, respectively. The EK Ca channel openers chlorzoxazone, zoxazolamine and 1-ethyl-2-benz-imidazolinone and the Ca2+-activated Cl- channel blocker niflumic acid activated the KCa current. In inside-out patches, the single-channel conductance was 17.7 pS in symmetrical K+ solutions. RT-PCR analysis showed transcripts of the murine IK1 channel (mIK1) in MAECs. The IKCa channel blockers inhibited the ATP-induced [Ca2+]i increase in MAECs and the endothelium-dependent relaxation of mouse aortic rings. In addition, the IK Ca channel openers augmented ATP-induced [Ca2+] i increase in MAECs and evoked endothelium-dependent relaxation of mouse aorta. These results suggest that an mIK1-like channel mediates the native IKCa current in MAECs and may contribute to endothelium-dependent relaxation by modulating MAEC [Ca2+] i.
DOI
10.1007/s00424-003-1201-1
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의과대학 > 의학과 > Journal papers
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