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1 Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655; and 2 Department of Physiology, University of Melbourne, Victoria 3010, Australia
To determine
the mechanism of fatty acid modulation of rabbit pulmonary artery
large-conductance Ca2+-activated K+
(BKCa) channel activity, we studied effects of fatty acids
and other lipids on channel activity in excised patches with
patch-clamp techniques. The structural features of the fatty acid
required to increase BKCa channel activity (or average
number of open channels, NPo) were identified to
be the negatively charged head group and a sufficiently long (C > 8) carbon chain. Positively charged lipids like sphingosine, which have
a sufficiently long alkyl chain (C 
8), produced a decrease in
NPo. Neutral and short-chain lipids did not
alter NPo. Screening of membrane surface charge
with high-ionic-strength bathing solutions (330 mM K+ or
130 mM K+, 300 mM Na+) did not alter the
modulation of the BKCa channel NPo
by fatty acids and other charged lipids, indicating that channel
modulation is unlikely to be due to an alteration of the membrane
electric field or the attraction of local counterions to the channel.
Fatty acids and other negatively charged lipids were able to modulate BKCa channel activity in bathing solutions containing 0 mM
Ca2+, 20 mM EGTA, suggesting that calcium is not required
for this modulation. Together, these results indicate that modulation
of BKCa channels by fatty acids and other charged lipids
most likely occurs by their direct interaction with the channel protein
itself or with some other channel-associated component.
arachidonic acid; sphingosine; calcium-activated potassium channel
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