The Influences of G Proteins, Ca2+, and K+ Channels on Electrical Field Stimulation in Cat Esophageal Smooth Muscle

Park, Junhong; Kim, Hyun Sik; Park, Sun Young; Im, Chaeuk; Jeong, Ji Hoon; Kim, In Kyeom; Sohn, Uy Dong

doi:10.4196/kjpp.2009.13.5.393

Cited by 5 publications

(7 citation statements)

References 42 publications

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“…Muscle contractions were recorded using an isometric force transducer. Low-frequency EFS induced only off contraction but induced on contraction in the presence of N G -nitro-L-arginine methyl ester, suggesting that NO acts as an inhibitory mediator in smooth muscle [3].…”

Section: Introductionmentioning

confidence: 99%

“…In vitro studies of human esophageal strips using direct activation of enteric motor neurons by electrical field stimulation (EFS) have shown that lower esophageal smooth muscle relaxation is mainly caused by NO released from inhibitory enteric motor neurons, whereas esophageal contraction is mainly caused by acetylcholine released from excitatory enteric motor neurons acting on muscarinic receptors located in the smooth muscle [3,[28][29][30]. Except for acetylcholine, other neurotransmitters influence EFS-induced contraction in esophageal smooth muscle.…”

Section: Introductionmentioning

confidence: 99%

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P2X and P2Y Receptors Mediate Contraction Induced by Electrical Field Stimulation in Feline Esophageal Smooth Muscle

Cho

Jang

Kim

et al. 2010

Korean J Physiol Pharmacol

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

P2X and P2Y Receptors Mediate Contraction Induced by Electrical Field Stimulation in Feline Esophageal Smooth Muscle

Cho

Jang

Kim

et al. 2010

Korean J Physiol Pharmacol

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“…In addition, ion currents generated via 4-AP-sensitive voltage-dependent K ＋ channels in muscle might participate in EFS-induced responses [12]. In addition, EFS-induced those responses can be mediated by the activations Gi or Gs proteins, and that L-type Ca 2＋ channel may be activated by G-protein alpha subunits, indicating that K ＋ and Ca 2＋ channel involve in the depolarization of esophageal smooth muscle [13]. Thus, studies are required to characterize the physiological regulation of Ca 2＋ channel and to investigate the effects of other K ＋ channels on EFS-induced on and off contractions.…”

Section: Introductionmentioning

confidence: 99%

MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle

Park

Shim

Kim

et al. 2010

Korean J Physiol Pharmacol

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W e have shown that myosin light chain kinase (MLCK) was required for the off-contraction in response to the electrical field stimulation (EFS) of feline esophageal smooth muscle. In this study, we investigated whether protein kinase C (PKC) may require the on-contraction in response to EFS using feline esophageal smooth muscle. The contractions were recorded using an isometric force transducer. On-contraction occurred in the presence of N G -nitro-L-arginine methyl ester (L-NAME), suggesting that nitric oxide acts as an inhibitory mediator in smooth muscle. The excitatory composition of both contractions was cholinergic dependent which was blocked by tetrodotoxin or atropine. The on-contraction was abolished in Ca 2＋ -free buffer but reappeared in normal Ca 2＋ -containing buffer indicating that the contraction was Ca 2＋ dependent. 4-aminopyridine (4-AP), voltage-dependent K＋ channel blocker, significantly enhanced on-contraction. Aluminum fluoride (a G-protein activator) increased on-contraction. Pertussis toxin (a Gi inactivator) and C3 exoenzyme (a rhoA inactivator) significantly decreased on-contraction suggesting that Gi or rhoA protein may be related with Ca 2＋ and K ＋ channel. ML-9, a MLCK inhibitor, significantly inhibited on-contraction, and chelerythrine (PKC inhibitor) affected on the contraction. These results suggest that endogenous cholinergic contractions activated directly by low-frequency EFS may be mediated by Ca 2＋ , and G proteins, such as Gi and rhoA, which resulted in the activation of MLCK, and PKC to produce the contraction in feline distal esophageal smooth muscle.

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“…1a). It has been reported that EFS-induced contraction in smooth muscle is nerve origin and cholinergic nerves are also responsible for contractions [20]. Then, the response of rat ileal smooth muscle to FLX was investigated initially.…”

Section: Resultsmentioning

confidence: 99%

“…However, the contraction of ileum muscle in mouse is mediated through the 5-HT 3 receptor [19]. Since there is a communication network between serotonin in the gut and the brain and spinal cord, it is possible that the drugs that are used for the brain such as antidepressants could influence serotonergic receptors in the GI tract [20]. However, little information concerning the effect of FLX on GI tract is available.…”

Section: Introductionmentioning

confidence: 99%

Signal Transduction Underlying the Inhibitory Mechanism of Fluoxetine on Electrical Field Stimulation Response in Rat Ileal Smooth Muscle

Khin

Zaw²,

Sohn³

2017

Pharmacology

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Fluoxetine (FLX), a well-known antidepressant drug under the class of selective serotonin reuptake inhibitor, exerts its action by inhibiting the reuptake of serotonin selectively. In some studies, it has been demonstrated that FLX relaxes the intestinal smooth muscle. In this study, we aimed at studying the signal transduction pathway underlying the muscle relaxation effect of FLX on electrically stimulated rat ileal muscle contraction. To investigate the possible mechanism involved, various antagonists were used. It was found that inhibition with L-N^G-nitroarginine methyl ester, ondansetron, GR113808 and bicuculline enhanced the relaxation effect of FLX. However, the effect of FLX was nullified under the presence of atropine, calcium channel modulator (calcium ionophore A23187), and potassium channel blockers (tetraethylammonium chloride, 4-aminopyridine and glybenclamide). Specific pathway-inhibiting antagonists, Y27632 (Rho-kinase inhibitor) and U73122 (phospholipase-C inhibitor) reversed the antagonistic effect of FLX, while ML-9 (myosin light chain kinase inhibitor) and chelerythrine (protein kinase C inhibitor) augmented the FLX-induced inhibition effect. Taken together, we concluded that FLX exerts the inhibitory effect on electric field stimulation response in rat ileal smooth muscle by the inhibition of muscarinic receptors, decrease of intracellular calcium level by inhibiting phospholipase C and opens the potassium channels.

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The Influences of G Proteins, Ca2+, and K+ Channels on Electrical Field Stimulation in Cat Esophageal Smooth Muscle

Cited by 5 publications

References 42 publications

P2X and P2Y Receptors Mediate Contraction Induced by Electrical Field Stimulation in Feline Esophageal Smooth Muscle

P2X and P2Y Receptors Mediate Contraction Induced by Electrical Field Stimulation in Feline Esophageal Smooth Muscle

MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle

Signal Transduction Underlying the Inhibitory Mechanism of Fluoxetine on Electrical Field Stimulation Response in Rat Ileal Smooth Muscle

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