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However, it is not clear whether some antiarrhythmics affect the activity of TREK-1. The TWIK-related potassium channel (TREK-1) can be regulated by different stimuli. Remodelling patterns, observed in disease models are discussed and compared to findings from clinical patients to assess the therapeutic potential of K2P channels. In the present review, expression, function, and regulation of cardiovascular K2P channels are summarized and compared among different species. Cardiovascular expression of other K2P channels has been described, functional evidence in cardiac tissue however remains sparse. Further, mechanoactive K2P2.1 (TREK-1) currents have been implicated in the development of cardiac hypertrophy, cardiac fibrosis and heart failure. Therefore, targeting K2P3.1 (TASK-1) channels might constitute an intriguing strategy for AF treatment. For example, upregulation of atrial specific K2P3.1 (TASK-1) currents in atrial fibrillation (AF) patients was shown to contribute to atrial action potential duration shortening, a key feature of AF-associated atrial electrical remodelling. In patients suffering from cardiovascular diseases, alterations in K2P-channel expression and function have been observed, suggesting functional significance and a potential therapeutic role of these ion channels. Their functional activity is controlled by a broad variety of different stimuli, like pH level, temperature, and mechanical stress but also by the presence of lipids or pharmacological agents. Members of the K2P channel family are widely expressed among different human cell types and organs where they were shown to regulate important physiological processes.
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Two-pore-domain potassium (K2P-) channels conduct outward K+ currents that maintain the resting membrane potential and modulate action potential repolarization. Note the prominent increase in open probability of hTREK1 on application of negative pressure through the patch pipette. The measured slope conductance was 95.7 9.4 pS (n 7). The reversal potential of hTREK1 shifted from 84 to 0 mV on changing the external K. c, single-channel current-voltage relationship obtained by measuring the unitary current amplitudes at varying potentials in symmetric and physiological K gradients. b, single hTREK1 channel current evoked in symmetrical K gradient by a ramp pulse depicted below the current tracing. The arrow points to the flickery shortduration closed state within the burst, and the asterisk marks the long interburst closed state. Note the presence of the two open conductance levels depicted by dotted lines. ii, part of the trace at 60 mV, illustrated at high resolution. Note the mild outward rectification of single hTREK1 channel. Shown are the two open conductances, O* (blocked, 2.9 pA) and O (unblocked, 6.8 pA), at hyperpolarized potential (60 mV) owing to the internal Mg 2 block. a, i, a single hTREK1 channel at varying membrane potentials (as indicated) in symmetrical K gradient showing reversal at 0 mV. Characterization of single hTREK1 channels in excised inside-out patches.