Indirect activation by internal calcium of chloride channels in endothelial cells.
The action of internal Ca2+ on Cl- channels in endothelial cells was studied by the whole-cell clamp technique in cultured human aortic endothelial cells. Intracellular Ca2+ application by break-in of a Ca(2+)-containing pipette solution produced an outward-rectifying Cl- current after a few minutes delay. The amplitude of the Cl- current increased with the increase in the internal Ca2+ concentration, producing a maximal Cl- conductance as large as 2 nS/pF at pCa 5. The increase of the Ca(2+)-induced Cl- conductance was also dependent on the internal ATP concentration. At pCa 5, the Cl conductance per cell was 61 nS at 5 mM ATP and 24 nS at 1 mM. The calmodulin antagonists trifluoperazine and W-7 blocked the Cl- channel reversibly. The results suggest that Ca2+ activates the Cl- channels indirectly via a calmodulin-mediated pathway, and that binding of ATP to the channel is a prerequisite for activation.
Watanabe
M
M
Department of Physiology, Juntendo University School of Medicine, Tokyo, Japan.
Yumoto
K
K
Ochi
R
R
D000255:Adenosine Triphosphate / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D018118:Chloride Channels / Q000502:physiology*; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004727:Endothelium; D006801:Humans; D018408:Patch-Clamp Techniques
D018118:Chloride Channels; D004533:Egtazic Acid; D000255:Adenosine Triphosphate; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium