Action of imipramine on activated ATP-sensitive K+ channels in interstitial cells of Cajal from murine small intestine

Choi, Seok; Park, Chan Guk; Kim, Man Yoo; Lim, Geon Han; Kim, Jin Ho; Yeum, Cheol Ho; Yoon, Pyung Jin; So, Insuk; Kim, Ki Whan; Jun, Jae Yeoul

doi:10.1016/j.lfs.2005.09.032

Cited by 11 publications

(10 citation statements)

References 33 publications

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“…However, we performed experiments in culture systems. So in culture systems, pinacidil decreased the frequency of the pacemaker potentials (Jun et al, 2005;Choi et al, 2006aChoi et al, , 2006bChoi et al, , 2006c. We think that the results obtained in native tissue may be more accurate considering that the interactions of platelet-derived growth factor receptor-α-positive (PDGFRα þ ) and enteric neurons might have an effect in native tissues.…”

Section: Discussionmentioning

confidence: 93%

“…Sulphonylurea receptors (SUR) can modulate pacemaker [Ca 2 þ ]i oscillations via voltage-independent mechanism(s), and also intestinal pacemaking and glucose control are closely associated with SUR (Nakayama et al, 2005). Additionally, imipramine (Tricyclic antidepressants) (Choi et al, 2006c), calcitonin gene-related peptide (Choi et al, 2008), phentolamine (Ahn et al, 2010) and imatinib mesylate could modulate the pacemaking activity in ICCs through ATP-sensitive K þ channels. The effects of GGT are very similar with those of noradrenaline on ICCs.…”

Section: Discussionmentioning

confidence: 99%

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The traditional herbal medicine, Ge-Gen-Tang, inhibits pacemaker potentials by nitric oxide/cGMP dependent ATP-sensitive K+ channels in cultured interstitial cells of Cajal from mouse small intestine

Lee

Gim

Shim

et al. 2015

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

The traditional herbal medicine, Ge-Gen-Tang, inhibits pacemaker potentials by nitric oxide/cGMP dependent ATP-sensitive K+ channels in cultured interstitial cells of Cajal from mouse small intestine

Lee

Gim

Shim

et al. 2015

Journal of Ethnopharmacology

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“…24,25) In ICC, deoxycholic acid inhibited pacemaker currents by activating K ATP channels through PGE2, 26) and imipramine inhibited the activated K ATP channels. 27) Also, K ATP channel was involved in the response of nitric oxide or calcitonin gene-related peptide on pacemaker activity. 28,29) In this study, we have demonstrated that pinacidil inhibits pacemaker potentials, which are antagonized by glibenclamide ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Kim

Chae

Kwon

et al. 2010

Biological & Pharmaceutical Bulletin

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The interstitial cells of Cajal (ICCs) are pacemakers in the gastrointestinal tract. The possibility of whether imatinib mesylate, a Kit receptor tyrosine kinase inhibitor, modulates pacemaker activities in the ICC was examined using the whole cell patch clamp technique. Imatinib decreased the amplitude of pacemaker potentials in a dose-dependent manner in current-clamp mode. Because the effects of imatinib on pacemaker potentials were the same as those of pinacidil, we examined the effect of glibenclamide on ICC exposed to imatinib. The effects of imatinib on pacemaker potentials were blocked by glibenclamide. To see whether the production of prostaglandins (PGs) is involved in the inhibitory effect of imatinib on pacemaker potentials, we tested the effects of naproxen (a non-selective cyclooxygenase inhibitor) and AH6809 (a prostaglandin EP1 and EP2 receptor antagonist). Naproxen and AH6809 blocked the inhibitory effects of imatinib on ICC. Butaprost (an EP2 receptor agonist) showed the actions on pacemaker potentials in the same manner as imatinib. However, SC 19220 (an EP1 receptor antagonist) has no effects. To investigate the involvement of cAMP and protein kinase A (PKA) in the effects of imatinib on ICC, SQ 22536 (an inhibitor of adenylate cyclase) and mPKAI (an inhibitor of myristoylated PKA) were used. Both SQ-22536 and mPKAI blocked the imatinib-mediated inhibition of pacemaker potentials. However, the protein kinase C (PKC) inhibitors did not block the imatinib-mediated inhibition of pacemaker potentials. These results indicate that imatinib inhibits the pacemaker potentials of ICC by activating ATP-sensitive K ؉ ؉ channels and PKA-dependent, PKC-independent manner.

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“…However, studies have revealed no effect of AMT on perception of rectal and esophageal distention (13), no effect of a single AMT dose on rectal compliance or visceral perception (14), and no alteration of perceptual responses to gastric distention (11). There does appear to be an effect on gastrointestinal motility, with slowed orocecal transit (12), inhibited muscular contraction in vitro (59), and inhibited ATP-sensitive K(+) channels in cultured murine interstitial cells of Cajal (60). What sensory or clinical impact these physiologic perturbations may have is difficult to say based on our current understanding of symptom generation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Amitriptyline on Gastric Sensorimotor Function and Postprandial Symptoms in Healthy Individuals: A Randomized, Double-Blind, Placebo-Controlled Trial

Bouras

Talley

Camilleri³

et al. 2008

The American Journal of Gastroenterology

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BACKGROUND Low-dose tricyclic antidepressants have been used to treat chronic somatic and gastrointestinal pain disorders, including refractory functional dyspepsia. However, there are only limited data on the effects of these drugs on upper gastrointestinal function. AIM To compare the effects of two doses of amitriptyline (AMT) and placebo on gastric accommodation, emptying, satiation, and postprandial symptoms in healthy volunteers. METHODS Using a parallel-group, double-blind, placebo-controlled design, 41 healthy volunteers were randomized to AMT 25 mg, AMT 50 mg, or placebo for 2 wk. During the final 3 days of therapy, the following end points were assessed: fasting and postprandial gastric volumes, 2- and 4-h gastric emptying, time and volume to maximum satiation using a nutrient drink test, and postprandial symptoms 30 min later using 10-cm visual analog scales. AMT and metabolite levels were measured. RESULTS AMT slowed gastric emptying at 2 h (median 75% for placebo, 57% for AMT 25 mg, 67% for AMT 50 mg; P = 0.037) and 4 h (median 98% for placebo, 96% for AMT 25 mg, 92% for AMT 50 mg; P = 0.003). AMT did not affect gastric volumes or satiation volume, but it did reduce nausea scores at 30 min in a dose-dependent manner (median 2.1 for placebo, 0.9 for AMT 25 mg, and 0.0 for AMT 50 mg; P = 0.009). CONCLUSION In healthy volunteers, AMT slows gastric emptying of solids, but it does not significantly affect gastric volumes or satiation. AMT reduces nausea after challenge with a high calorie liquid load.

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Action of imipramine on activated ATP-sensitive K+ channels in interstitial cells of Cajal from murine small intestine

Cited by 11 publications

References 33 publications

The traditional herbal medicine, Ge-Gen-Tang, inhibits pacemaker potentials by nitric oxide/cGMP dependent ATP-sensitive K+ channels in cultured interstitial cells of Cajal from mouse small intestine

The traditional herbal medicine, Ge-Gen-Tang, inhibits pacemaker potentials by nitric oxide/cGMP dependent ATP-sensitive K+ channels in cultured interstitial cells of Cajal from mouse small intestine

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Effects of Amitriptyline on Gastric Sensorimotor Function and Postprandial Symptoms in Healthy Individuals: A Randomized, Double-Blind, Placebo-Controlled Trial

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