The reactivity of serotonin, acetylcholine and kcl-induced contractions to relaxant agents in the rat gastric fundus

Buharalioğlu, C. Kemal; Akar, Fatma

doi:10.1006/phrs.2002.0950

Cited by 18 publications

(12 citation statements)

References 26 publications

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“…[49] As serotonergic medications could be responsible for causing secondary RBD [37], it is important to also consider this mechanism. Serotonin agonism has shown to induce muscle tonicity in animal gastric intestinal tract [50,51] and human skeletal muscle. [52] Attenuation of serotonin induced contraction was demonstrated with pretreatment of nifedipine, cromakalim, dizoxide, caffeine and sodium nitroprusside; but acetylcholine induced contractions were refractory to these agents, suggesting two distinct contraction pathways.…”

Section: 1 Discussionmentioning

confidence: 99%

“…[52] Attenuation of serotonin induced contraction was demonstrated with pretreatment of nifedipine, cromakalim, dizoxide, caffeine and sodium nitroprusside; but acetylcholine induced contractions were refractory to these agents, suggesting two distinct contraction pathways. [50] Due to these data, the pathophysiology of RBD could be multifactorial, in which more research is necessary.…”

Section: 1 Discussionmentioning

confidence: 99%

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Melatonin therapy for REM sleep behavior disorder: a critical review of evidence

et al. 2015

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REM sleep behavior disorder (RBD) is a parasomnia associated with dream enactment often involving violent or potentially injurious behaviors during REM sleep that is strongly associated with synucleinopathy neurodegeneration. Clonazepam has long been suggested as the first-line treatment option for RBD. However, evidence supporting melatonin therapy is expanding. Melatonin appears to be beneficial for the management of RBD with reductions in clinical behavioral outcomes and decrease in muscle tonicity during REM sleep. Melatonin also has a favorable safety and tolerability profile over clonazepam with limited potential for drug-drug interactions, an important consideration especially in elderly individuals with RBD receiving polypharmacy. Prospective clinical trials are necessary to establish evidence-basis for melatonin and clonazepam as RBD therapies.

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Section: 1 Discussionmentioning

confidence: 99%

Section: 1 Discussionmentioning

confidence: 99%

Melatonin therapy for REM sleep behavior disorder: a critical review of evidence

et al. 2015

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“…Thus, molecular identification of potential K + channel candidates has come primarily from localization of proteins in parietal cells and assessment of the effects of specific channel blockers on acid secretion [15,28,37,44]. While several inward rectifier and voltage-gated K + channels have been identified using this approach [8,14,15,22], it is unclear whether these channels were involved in K + recycling or in other tasks such as maintaining membrane potential necessary to drive Cl − secretion [4,35,49]. The results presented in this report are consistent with the expression of the K ir 1.1 K + channel being essential for normal gastric acidification.…”

Section: Discussionmentioning

confidence: 99%

“…Proton secretion was assessed in BCECF-loaded parietal cells by following cell pH (pH i ) recovery after acid loading with 20 mM NH4 Cl in the absence of extracellular sodium to inhibit NHE activity. a Overlay of two representative intracellular pH i tracings after NH 4 Cl induced intracellular acidification from wild-type (Kcnj1 +/+ ) and K ir 1.1-deficient (Kcnj1 −/− ) mice in the presence of 100 μM histamine.…”

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confidence: 99%

Kir1.1 (ROMK) and Kv7.1 (KCNQ1/KvLQT1) are essential for normal gastric acid secretion: importance of functional Kir1.1

Vucic

Alfadda

MacGregor

et al. 2014

Pflugers Arch - Eur J Physiol

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Potassium channels comprise the apical leak pathway supplying extracellular K(+) for exchange with protons by the gastric H(+), K(+)-ATPase and provide potential therapeutic targets for inhibiting gastric acid secretion. The Kir1.1 (ROMK) potassium channel mediates the high capacity K(+) recycling necessary for NaCl reabsorption in the thick ascending limb of the kidney, and this channel exhibits functional and regulatory characteristic well suited for K(+) recycling by gastric parietal cells. We report here that Kir1.1 channels are required for gastric acid secretion and that this channel participates with Kv7.1 (KCNQ1/KvLQT1) in the potassium recycling process. We show that Kir1.1 colocalizes with the β-subunit of H(+), K(+)-ATPase in gastric parietal cells of Kir1.1 wild-type mice. In Kir1.1-deficient mice, gastric mucosal morphology, as well as parietal cell number, proliferation index, and ultrastructure were normal but secretagogue-stimulated gastric acid secretion in whole stomach and perfused gastric glands was absent. Luminal application of potassium-restored acid secretion in perfused gastric glands from Kir1.1-deficient as well as barium-blocked wild-type mice. In wild-type mice, both luminal Tertiapin-Q, an inhibitor of Kir1.1, as well as XE991, an inhibitor of Kv7.1, reduced proton secretion. We propose that Kir1.1 and Kv7.1 channels collaborate in potassium and current recycling across the apical pole of parietal cells.

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“…This stimulus initially failed to induce sustained contractions, but contractions were subsequently triggered by increasing concentrations of CaCl 2 in the bath solution. High K + concentrations depolarize smooth muscle cells and open voltage‐operated L‐type Ca 2+ channels (Buharalioğlu & Akar, ; Kirschstein et al . ).…”

Section: Discussionmentioning

confidence: 99%

Extracellular acidosis selectively inhibits pharmacomechanical coupling induced by carbachol in strips of rat gastric fundus

Oliveira

Batista‐Lima

Carvalho

et al. 2017

Experimental Physiology

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What is the central question of this study? Acute acidosis that results from short-term exercise is involved in delayed gastric emptying in rats and the lower responsiveness of gastric fundus strips to carbachol. Does extracellular acidosis decrease responsiveness to carbachol in tissues of sedentary rats? How? What is the main finding and its importance? Extracellular acidosis inhibits cholinergic signalling in the rat gastric fundus by selectively influencing the G protein signalling pathway. Acute acidosis that results from short-term exercise delays gastric emptying in rats and decreases the responsiveness to carbachol in gastric fundus strips. The regulation of cytosolic Ca concentrations appears to be a mechanism of action of acidosis. The present study investigated the way in which acidosis interferes with gastric smooth muscle contractions. Rat gastric fundus isolated strips at pH 6.0 presented a lower magnitude of carbachol-induced contractions compared with preparations at pH 7.4. This lower magnitude was absent in carbachol-stimulated duodenum and KCl-stimulated gastric fundus strips. In Ca -free conditions, repeated contractions that were induced by carbachol progressively decreased, with no influence of extracellular pH. In fundus strips, CaCl -induced contractions were lower at pH 6.0 than at pH 7.4 but only when stimulated in the combined presence of carbachol and verapamil. In contrast, verapamil-sensitive contractions that were induced by CaCl in the presence of KCl did not change with pH acidification. In Ca store-depleted preparations that were treated with thapsigargin, the contractions that were induced by extracellular Ca restoration were smaller at pH 6.0 than at pH 7.4, but relaxation that was induced by SKF-96365 (an inhibitor of store-operated Ca entry) was unaltered by extracellular acidification. At pH 6.0, the phospholipase C inhibitor U-73122 relaxed carbachol-induced contractions less than at pH 7.4, and this phenomenon was absent in tissue that was treated with the RhoA kinase blocker Y-27632. Thus, extracellular acidosis inhibited pharmacomechanical coupling in gastric fundus by selectively inhibiting the G protein signalling pathway, whereas electromechanical coupling remained functionally preserved.

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The reactivity of serotonin, acetylcholine and kcl-induced contractions to relaxant agents in the rat gastric fundus

Cited by 18 publications

References 26 publications

Melatonin therapy for REM sleep behavior disorder: a critical review of evidence

Melatonin therapy for REM sleep behavior disorder: a critical review of evidence

Kir1.1 (ROMK) and Kv7.1 (KCNQ1/KvLQT1) are essential for normal gastric acid secretion: importance of functional Kir1.1

Extracellular acidosis selectively inhibits pharmacomechanical coupling induced by carbachol in strips of rat gastric fundus

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