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

Lee JY, Ko EJ, Ahn KD, Kim S, Rhee PL - Am. J. Physiol. Gastrointest. Liver Physiol. (2015)

Bottom Line: 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.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.

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Affiliation: Samsung Biomedical Research Institute and.

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Effect of Ba2+ on the slow wave potential in HGCS. A: a representative trace showed that Ba2+ (50–500 μM) significantly depolarized HGCS. B–D: expanded time scale from A in control (B), low concentration of Ba2+ (50 μM) (C), and high concentration of Ba2+ (500 μM) (D), respectively. E and F: summarized data showed significant changes in the resting membrane potential (RMP, E) and the slow wave amplitude (F) from 5 samples in each concentration. **P < 0.01; ***P < 0.001.
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Figure 5: Effect of Ba2+ on the slow wave potential in HGCS. A: a representative trace showed that Ba2+ (50–500 μM) significantly depolarized HGCS. B–D: expanded time scale from A in control (B), low concentration of Ba2+ (50 μM) (C), and high concentration of Ba2+ (500 μM) (D), respectively. E and F: summarized data showed significant changes in the resting membrane potential (RMP, E) and the slow wave amplitude (F) from 5 samples in each concentration. **P < 0.01; ***P < 0.001.

Mentions: Kir can be blocked by low concentration of Ba2+ (6, 19). Bath application of Ba2+ (50 μM) depolarized HGCS from −72 ± 3 mV to −61 ± 3 mV (P < 0.001, n = 5, Fig. 5, A–C). A higher concentration Ba2+ (500 μM) induced strong depolarization of HGCS to −51 ± 2 mV (P < 0.001, n = 5, Fig. 5, A and E). Ba2+ also significantly decreased the amplitude (Fig. 5F) of SWP. Ba2+ (500 μM, n = 3 of 5 experiments) completely abolished SWP with strong depolarization. Therefore, we could not analyze the effect of Ba2+ on the duration of SWP. These data suggest that Kir channels are involved in regulating RMP of HGCS.


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

Lee JY, Ko EJ, Ahn KD, Kim S, Rhee PL - Am. J. Physiol. Gastrointest. Liver Physiol. (2015)

Effect of Ba2+ on the slow wave potential in HGCS. A: a representative trace showed that Ba2+ (50–500 μM) significantly depolarized HGCS. B–D: expanded time scale from A in control (B), low concentration of Ba2+ (50 μM) (C), and high concentration of Ba2+ (500 μM) (D), respectively. E and F: summarized data showed significant changes in the resting membrane potential (RMP, E) and the slow wave amplitude (F) from 5 samples in each concentration. **P < 0.01; ***P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4385896&req=5

Figure 5: Effect of Ba2+ on the slow wave potential in HGCS. A: a representative trace showed that Ba2+ (50–500 μM) significantly depolarized HGCS. B–D: expanded time scale from A in control (B), low concentration of Ba2+ (50 μM) (C), and high concentration of Ba2+ (500 μM) (D), respectively. E and F: summarized data showed significant changes in the resting membrane potential (RMP, E) and the slow wave amplitude (F) from 5 samples in each concentration. **P < 0.01; ***P < 0.001.
Mentions: Kir can be blocked by low concentration of Ba2+ (6, 19). Bath application of Ba2+ (50 μM) depolarized HGCS from −72 ± 3 mV to −61 ± 3 mV (P < 0.001, n = 5, Fig. 5, A–C). A higher concentration Ba2+ (500 μM) induced strong depolarization of HGCS to −51 ± 2 mV (P < 0.001, n = 5, Fig. 5, A and E). Ba2+ also significantly decreased the amplitude (Fig. 5F) of SWP. Ba2+ (500 μM, n = 3 of 5 experiments) completely abolished SWP with strong depolarization. Therefore, we could not analyze the effect of Ba2+ on the duration of SWP. These data suggest that Kir channels are involved in regulating RMP of HGCS.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Samsung Biomedical Research Institute and.

Show MeSH
Related in: MedlinePlus