PMID- 14648123
OWN - NLM
STAT- MEDLINE
DCOM- 20040927
LR  - 20181113
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 447
IP  - 4
DP  - 2004 Jan
TI  - Characteristics and a functional implication of Ca(2+)-activated K(+) current in 
      mouse aortic endothelial cells.
PG  - 426-35
AB  - We employed the patch-clamp technique to investigate a Ca(2+)-activated K(+) 
      (K(Ca)) current in cultured mouse aortic endothelial cells (MAECs). In the 
      whole-cell mode, an increase in cytosolic [Ca(2+)] ([Ca(2+)](i)) to 2 micro M 
      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 K(Ca) current. The Hill coefficient (4) and EC(50) (740 nM) were obtained 
      from the current/[Ca(2+)](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(+) (IK(Ca)) channel blockers charybdotoxin (50 nM), clotrimazole (10 micro M) 
      and econazole (10 micro M) inhibited the K(Ca) 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 IK(Ca) 
      channel openers chlorzoxazone, zoxazolamine and 1-ethyl-2-benz-imidazolinone and 
      the Ca(2+)-activated Cl(-) channel blocker niflumic acid activated the K(Ca) 
      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 IK(Ca) channel blockers inhibited the ATP-induced 
      [Ca(2+)](i) increase in MAECs and the endothelium-dependent relaxation of mouse 
      aortic rings. In addition, the IK(Ca) channel openers augmented ATP-induced 
      [Ca(2+)](i) increase in MAECs and evoked endothelium-dependent relaxation of 
      mouse aorta. These results suggest that an mIK1-like channel mediates the native 
      IK(Ca) current in MAECs and may contribute to endothelium-dependent relaxation by 
      modulating MAEC [Ca(2+)](i).
FAU - Ahn, Seung Cheol
AU  - Ahn SC
AD  - Department of Physiology, College of Medicine, Dankook University, Cheonan, 
      Republic of Korea.
FAU - Seol, Geun Hee
AU  - Seol GH
FAU - Kim, Ji Aee
AU  - Kim JA
FAU - Suh, Suk Hyo
AU  - Suh SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20031126
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Chloride Channels)
RN  - 0 (Muscle Relaxants, Central)
RN  - 0 (Potassium Channel Blockers)
RN  - 0 (Potassium Channels, Calcium-Activated)
RN  - 4U5MP5IUD8 (Niflumic Acid)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Aorta/*anatomy & histology
MH  - Calcium/*metabolism
MH  - Cells, Cultured
MH  - Chloride Channels/antagonists & inhibitors
MH  - Endothelial Cells/cytology/drug effects/*metabolism
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Female
MH  - Male
MH  - Mice
MH  - Muscle Relaxants, Central/pharmacology
MH  - Muscle Relaxation/drug effects/physiology
MH  - Niflumic Acid/pharmacology
MH  - Patch-Clamp Techniques
MH  - Potassium Channel Blockers/pharmacology
MH  - Potassium Channels, Calcium-Activated/antagonists & 
      inhibitors/genetics/*metabolism
EDAT- 2003/12/03 05:00
MHDA- 2004/09/28 05:00
CRDT- 2003/12/03 05:00
PHST- 2003/09/07 00:00 [received]
PHST- 2003/10/14 00:00 [accepted]
PHST- 2003/12/03 05:00 [pubmed]
PHST- 2004/09/28 05:00 [medline]
PHST- 2003/12/03 05:00 [entrez]
AID - 10.1007/s00424-003-1201-1 [doi]
PST - ppublish
SO  - Pflugers Arch. 2004 Jan;447(4):426-35. doi: 10.1007/s00424-003-1201-1. Epub 2003 
      Nov 26.