Send to

Choose Destination
Am J Physiol Cell Physiol. 2000 Oct;279(4):C1107-15.

Potent inhibition of the aortic smooth muscle maxi-K channel by clinical doses of ethanol.

Author information

Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.


We investigated the effects of clinically relevant ethanol concentrations (5-20 mM) on the single-channel kinetics of bovine aortic smooth muscle maxi-K channels reconstituted in lipid bilayers (1:1 palmitoyl-oleoyl-phosphatidylethanolamine: palmitoyl-oleoyl-phosphatidylcholine). Ethanol at 10 and 20 mM decreased the channel open probability (P(o)) by 75 +/- 20.3% mainly by increasing the mean closed time (+82 to +960%, n = 7). In some instances, ethanol also decreased the mean open time (-40.8 +/- 22. 5%). The P(o)-voltage relation in the presence of 20 mM ethanol exhibited a rightward shift in the midpoint of voltage activation (DeltaV(1/2) congruent with 17 mV), a slightly steeper relationship (change in slope factor, Deltak, congruent with -2.5 mV), and a decreased maximum P(o) (from approximately 0.82 to approximately 0. 47). Interestingly, channels inhibited by ethanol at low Ca(2+) concentrations (2.5 microM) were very resistant to ethanol in the presence of increased Ca(2+) (>/= 20 microM). Alcohol consumption in clinically relevant amounts may alter the contribution of maxi-K channels to the regulation of arterial tone.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center