Abstract
BK(maxi K) Ca2+- and voltage-activated K+ channels play a role in shaping muscle and neuronal excitability. Inhibition of BK channels lowers heart rate in intact rodents and isolated hearts, suggesting a novel role in heart function. Lai et al (Am J Physiol 2014;[Epub ahead of print], PMID 25172903) examined the underlying mechanism. They recorded ECGs from mice injected with paxilline (PAX), a membrane-permeable BK channel antagonist, and examined changes in cardiac conduction. PAX reduced heart rate (HR) in WT but not BK knockout(Kcnma1–/–) mice. HR decrease was associated with slowed cardiac pacing due to prolongation of the sinus interval. Action potential rate of sinoatrial node cells (SANs) was reduced by 55% ± 15% and 28% ± 9% with application of PAX and iberiotoxin, respectively. BK channel immunoreactivity and PAX-sensitive currents were identified in SANs, and BK channels cloned from SANs recapitulated similar activation as the PAX-sensitive current. The authors suggest that BK channels are in SANs, and loss of BK current decreases SAN automaticity, consistent with slowed sinus pacing after PAX injection in vivo.
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