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Characteristics and a functional implication of Ca2+-activated K+ current in mouse aortic endothelial cells
- Characteristics and a functional implication of Ca2+-activated K+ current in mouse aortic endothelial cells
- Ahn S.C.; Seol G.H.; Kim J.A.; Suh S.H.
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- Pflugers Archiv European Journal of Physiology
- vol. 447, no. 4, pp. 426 - 435
- SCI; SCIE; SCOPUS
- 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.
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