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J Physiol Volume 586, Number 15, 3645-3656, August 1, 2008 DOI: 10.1113/jphysiol.2008.153395
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CARDIOVASCULAR

Temperature-sensitive TREK currents contribute to setting the resting membrane potential in embryonic atrial myocytes

 Hengtao Zhang1, Neal Shepherd1 and Tony L. Creazzo1

1 Jean and George Brumley, Jr. Neonatal-Perinatal Research Institute, Department of Pediatrics/Division of Neonatology, Duke University Medical Center, Box 3179, Durham, NC 27710, USA

TREK channels belong to the superfamily of two-pore-domain K+ channels and are activated by membrane stretch, arachidonic acid, volatile anaesthetics and heat. TREK-1 is highly expressed in the atrium of the adult heart. In this study, we investigated the role of TREK-1 and TREK-2 channels in regulating the resting membrane potential (RMP) of isolated chicken embryonic cardiac myocytes. At room temperature, the average RMP of embryonic day (ED) 11 atrial myocytes was –22 ± 2 mV. Raising the temperature to 35°C hyperpolarized the membrane to –69 ± 2 mV and activated a large outwardly rectifying K+ current that was relatively insensitive to conventional K+ channel inhibitors (TEA, 4-AP and Ba2+) but completely inhibited by tetracaine (200 µM), an inhibitor of TREK channels. The heat-induced hyperpolarization was mimicked by 10 µM arachidonic acid, an agonist of TREK channels. There was little or no inwardly rectifying K+ current (IK1) in the ED11 atrial cells. In marked contrast, ED11 ventricular myocytes exhibited a normal RMP (–86.1 ± 3.4 mV) and substantial IK1, but no temperature- or tetracaine-sensitive K+ currents. Both RT-PCR and real-time PCR further demonstrated that TREK-1 and TREK-2 are highly and almost equally expressed in ED11 atrium but much less expressed in ED11 ventricle. In addition, immunofluorescence demonstrated TREK-1 protein in the membrane of atrial myocytes. These data indicate the presence and function of TREK-1 and TREK-2 in the embryonic atrium. Moreover, we demonstrate that TREK-like currents have an essential role in determining membrane potential in embryonic atrial myocytes, where IK1 is absent.

(Received 29 February 2008; accepted after revision 12 June 2008; first published online 19 June 2008)
Corresponding author H. Zhang: Jean and George Brumley, Jr. Neonatal-Perinatal Research Institute, Department of Pediatrics/Division of Neonatology, Duke University Medical Center, Box 3179, Durham, NC 27710, USA. Email: zht{at}duke.edu

This paper has online supplemental material.






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