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Am J Physiol Cell Physiol 279: C1107-C1115, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 4, C1107-C1115, October 2000

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

F. S. Walters, M. Covarrubias, and J. S. Ellingson

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

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 (Po) 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 Po-voltage relation in the presence of 20 mM ethanol exhibited a rightward shift in the midpoint of voltage activation (Delta V1/2 congruent  17 mV), a slightly steeper relationship (change in slope factor, Delta k, congruent  -2.5 mV), and a decreased maximum Po (from ~0.82 to ~0.47). Interestingly, channels inhibited by ethanol at low Ca2+ concentrations (2.5 µM) were very resistant to ethanol in the presence of increased Ca2+ (>=  20 µM). Alcohol consumption in clinically relevant amounts may alter the contribution of maxi-K channels to the regulation of arterial tone.

calcium dependent; voltage-gated potassium channels; planar lipid bilayer; arterial tone; alcohol


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