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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.

View Article: PubMed Central - PubMed

Affiliation: Samsung Biomedical Research Institute and.

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Effect of apamin on the slow wave potential in HGCS. A: a representative trace showed that apamin (300 nM and 1 μM) had no effect on the slow wave potentials in HGCS. B–D: expanded time scale from A in control (B), apamin (300 nM) presence (C), and apamin (1 μM) presence (D), respectively. E–G: summarized data showed no significant changes in the resting membrane potential (RMP, E) but no significance on the slow wave amplitude (F) and half-duration of slow wave potentials (G) from 5 samples in each concentration.
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Figure 4: Effect of apamin on the slow wave potential in HGCS. A: a representative trace showed that apamin (300 nM and 1 μM) had no effect on the slow wave potentials in HGCS. B–D: expanded time scale from A in control (B), apamin (300 nM) presence (C), and apamin (1 μM) presence (D), respectively. E–G: summarized data showed no significant changes in the resting membrane potential (RMP, E) but no significance on the slow wave amplitude (F) and half-duration of slow wave potentials (G) from 5 samples in each concentration.

Mentions: Apamin, a SK channel blocker, is known to induce depolarization in various regions of gastrointestinal smooth muscles (19). However, it has also been reported that apamin had no effect on the RMP in guinea pig antrum (19). The effect of apamin in HGCS has not been studied. Apamin (300 nM–1 μM, n = 5 each concentration) did not affect the RMP, amplitude, and frequency of SWP in HGCS (Fig. 4), suggesting that the basal activation of SK channels in regulating RMP is negligible.


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 apamin on the slow wave potential in HGCS. A: a representative trace showed that apamin (300 nM and 1 μM) had no effect on the slow wave potentials in HGCS. B–D: expanded time scale from A in control (B), apamin (300 nM) presence (C), and apamin (1 μM) presence (D), respectively. E–G: summarized data showed no significant changes in the resting membrane potential (RMP, E) but no significance on the slow wave amplitude (F) and half-duration of slow wave potentials (G) from 5 samples in each concentration.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Effect of apamin on the slow wave potential in HGCS. A: a representative trace showed that apamin (300 nM and 1 μM) had no effect on the slow wave potentials in HGCS. B–D: expanded time scale from A in control (B), apamin (300 nM) presence (C), and apamin (1 μM) presence (D), respectively. E–G: summarized data showed no significant changes in the resting membrane potential (RMP, E) but no significance on the slow wave amplitude (F) and half-duration of slow wave potentials (G) from 5 samples in each concentration.
Mentions: Apamin, a SK channel blocker, is known to induce depolarization in various regions of gastrointestinal smooth muscles (19). However, it has also been reported that apamin had no effect on the RMP in guinea pig antrum (19). The effect of apamin in HGCS has not been studied. Apamin (300 nM–1 μM, n = 5 each concentration) did not affect the RMP, amplitude, and frequency of SWP in HGCS (Fig. 4), suggesting that the basal activation of SK channels in regulating RMP is negligible.

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