The role of K⁺ conductances in regulating membrane excitability in human gastric corpus smooth muscle

• Published in: American journal of physiology: Gastrointestinal and liver physiology 2015-04, Vol.308 (7), p.G625-G633
• Main Authors: Lee, Ji Yeon, Ko, Eun-Ju, Ahn, Ki Duck, Kim, Sung, Rhee, Poong-Lyul
• Format: Article
• Language: English
• Subjects: Adenosine triphosphatase; Cells; ERG1 Potassium Channel; Ether-A-Go-Go Potassium Channels - metabolism; Female; Gastrointestinal Motility - drug effects; Humans; KATP Channels - metabolism; Male; Membrane Potentials; Membranes; Microelectrodes; Middle Aged; Muscle, Smooth - drug effects; Muscle, Smooth - metabolism; Neuroregulation and Motility; Patch-Clamp Techniques; Potassium - metabolism; Potassium Channel Blockers - pharmacology; Potassium Channels, Inwardly Rectifying - drug effects; Potassium Channels, Inwardly Rectifying - genetics; Potassium Channels, Inwardly Rectifying - metabolism; Potassium Channels, Voltage-Gated - drug effects; Potassium Channels, Voltage-Gated - genetics; Potassium Channels, Voltage-Gated - metabolism; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Small-Conductance Calcium-Activated Potassium Channels - metabolism; Smooth muscle; Stomach - drug effects; Stomach - metabolism; Time Factors
• ISSN: 0193-1857; 1522-1547
• DOI: 10.1152/ajpgi.00220.2014

Changes in resting membrane potential (RMP) regulate membrane excitability. K(+) conductance(s) are one of the main factors in regulating RMP. The functional role of K(+) conductances has not been studied the in human gastric corpus smooth muscles (HGCS). To examine the role of K(+) channels in regulation of RMP in HGCS we employed microelectrode recordings, patch-clamp, and molecular approaches. Tetraethylammonium and charybdotoxin did not affect the RMP, suggesting that BK channels are not involved in regulating RMP. Apamin, a selective small conductance Ca(2+)-activated K(+) channel (SK) blocker, did not show a significant effect on the membrane excitability. 4-Aminopyridine, a Kv channel blocker, caused depolarization and increased the duration of slow wave potentials. 4-Aminopyridine also inhibited a delayed rectifying K(+) current in isolated smooth muscle cells. End-product RT-PCR gel detected Kv1.2 and Kv1.5 in human gastric corpus muscles. Glibenclamide, an ATP-sensitive K(+) channel (KATP) blocker, did not induce depolarization, but nicorandil, a KATP opener, hyperpolarized HGCS, suggesting that KATP are expressed but not basally activated. Kir6.2 transcript, a pore-forming subunit of KATP was expressed in HGCS. A low concentration of Ba(2+), a Kir blocker, induced strong depolarization. Interestingly, Ba(2+)-sensitive currents were minimally expressed in isolated smooth muscle cells under whole-cell patch configuration. KCNJ2 (Kir2.1) transcript was expressed in HGCS. Unique K(+) conductances regulate the RMP in HGCS. Delayed and inwardly rectifying K(+) channels are the main candidates in regulating membrane excitability in HGCS. With the development of cell dispersion techniques of interstitial cells, the cell-specific functional significance will require further analysis.