Potent inhibition of the aortic smooth muscle maxi-K channel by clinical doses of ethanol.
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.[1]References
- Potent inhibition of the aortic smooth muscle maxi-K channel by clinical doses of ethanol. Walters, F.S., Covarrubias, M., Ellingson, J.S. Am. J. Physiol., Cell Physiol. (2000) [Pubmed]
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