Effect of misoprostol on histamine-stimulated acid secretion and cyclic AMP formation in isolated canine parietal cells

Tsai, Bie Shung; Kessler, L.K.; Butchko, G M; Bauer, R. F.

doi:10.1007/bf01297192

Cited by 18 publications

(7 citation statements)

References 23 publications

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“…The EP 3 receptor has at least four splicing variants coupled with different signaling pathways (14). It has also been reported that PGE 2 and its analog inhibited acid secretion as well as cAMP production stimulated by histamine in parietal cells (27,35). In addition, activation of the EP 3D receptor causes an elevation of intracellular Ca 2ϩ by stimulating G q protein.…”

Section: Discussionmentioning

confidence: 99%

Dual action of prostaglandin E₂ on gastric acid secretion through different EP-receptor subtypes in the rat

Kato

Aihara

Yoshii

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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We examined the role of prostaglandin E (EP) receptor subtypes in the regulation of gastric acid secretion in the rat. Under urethane anesthesia, the stomach was superfused with saline, and the acid secretion was determined at pH 7.0 by adding 50 mM NaOH. The acid secretion was stimulated by intravenous infusion of histamine or pentagastrin. Various EP agonists were administered intravenously, whereas EP antagonists were given subcutaneously 30 min or intravenously 10 min before EP agonists. PGE(2) suppressed the acid secretion stimulated by either histamine or pentagastrin in a dose-dependent manner. The acid inhibitory effect of PGE(2) was mimicked by sulprostone (EP(1)/EP(3) agonist) but not butaprost (EP(2) agonist) or AE1-329 (EP(4) agonist). The inhibitory effect of sulprostone, which was not affected by ONO-8711 (EP(1) antagonist), was more potent against pentagastrin- (50% inhibition dose: 3.6 mug/kg) than histamine-stimulated acid secretion (50% inhibition dose: 18.0 mug/kg). Pentagastrin increased the luminal release of histamine, and this response was also inhibited by sulprostone. On the other hand, AE1-329 (EP(4) agonist) stimulated the acid secretion in vagotomized animals with a significant increase in luminal histamine. This effect of AE1-329 was totally abolished by cimetidine as well as AE3-208 (EP(4) antagonist). These results suggest that PGE(2) has a dual effect on acid secretion: inhibition mediated by EP(3) receptors and stimulation through EP(4) receptors. The former effect may be brought about by suppression at both parietal and enterochromaffin-like cells, whereas the latter effect may be mediated by histamine released from enterochromaffin-like cells.

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Section: Discussionmentioning

confidence: 99%

Dual action of prostaglandin E₂ on gastric acid secretion through different EP-receptor subtypes in the rat

Kato

Aihara

Yoshii

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Natural and synthetic PGs have been shown to be potent inhibitors of gastric acid secretion and offer protection against peptic ulcers in animals and humans (26)(27)(28)(29)(30)(31). PG induced cytoprotective effects may involve increased blood flow (32,33), bicarbonate secretion (34), mucus release (35), restoration of active sodium transport (36), decrease in back diffusion of acid or local stimulation of surface-active phospholipids (37), and maintenace of normal mucosal levels of DNA, RNA or protein (38).…”

Section: Discussionmentioning

confidence: 99%

Different modes of inhibition of rat gastric mucosal 6-keto-PGF1.ALPHA. production by indomethacin, aspirin and aminopyrine.

Nishikawa¹,

Tomori

Yamashita

et al. 1989

Jpn.J.Pharmacol

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Abstract-The actions of aminopyrine on rat gastric mucosal cyclooxygenase activity in vitro were investigated and compared with those of the cyclooxygenase the back-diffusion of H+ through the mucosa, increased the loss of H+ from the lumen, and consequently reduced H+ secretion. The analgesic, antipyretic and anti-inflam matory properties and the PG synthesis inhibiting activities of these drugs have been extensively studied, but little is known about the mechanisms underlying ulcerogenesis in the gastrointestinal tract. The present study compared the effects of aminopyrine, in domethacin and aspirin on rat gastric mucosal cyclooxygenase activity under various experi mental conditions in order to try to establish the mechanisms of ulcerogenesis. Materials and MethodsPreparation of enzyme: Male Wistar rats weighing 150-250 g were killed by ex sanguination after a blow on the head. Following removal of their stomachs, mucosal sections were prepared by separating the overlying muscle by blistering (15). This pro cedure involved inserting the tip of a fine needle (26 gauge) between the muscle and mucosa and injecting 20 mM Tris-HCI buffer (pH 7.4). The raised muscle layer was then carefully cut away. The parts of the mucosal membranes were gently homogenized (200 rpm/min) in a glass-Teflon homogenizer with ten volumes of 50 mM potassium phosphate buffer (pH 7.4). All procedures were perfor med at 0-3'C. The homogenates were used as the source of the enzyme (cyclooxy genase). The enzyme was incubated at 37°C for 6 min, after which the enzyme activity was stopped by addition of 50 Id of ice-cold 2 M citric acid. The mixture was centrifuged at 20,000 g for 10 min at 0-3°C and then assessed for the production of 6-keto-PGF1a (the stable breakdown product of PG12) using radioimmunoassay kits (16). The results were expressed as ng (6-keto-PGF1a)/mg mucosal protein and as the percentage of inhibition of the control value. Mucosal protein concen tration was determined by the method of Lowry et al. (17) with bovine serum albumin as a standard.Reaction medium: Unless otherwise stated, determination of cyclooxygenase activity was carried out at 37°C in a 1-ml reaction mixture of arachidonic acid (2 x 10-5 M), enzymes (0.7 mg gastric mucosal protein/ml), hy droquinone (4x10-4 M), glutathione (5x10-4 M), various concentrations of indomethacin, aspirin or aminopyrine, ethanol (1.0%, v/v) and potassium phosphate buffer (50 mM, pH 7.4). The pH value of the incubation medium was always confirmed to be pH 7.4 before the start of incubation or pre-incubation.Ethanol, used as a solvent for arachidonic acid and inhibitors, had no effect on the reaction at the final concentration (2.0%, v/v) employed. Effects of indomethacin, aspirin and aminopyrine on cyclooxygenase activity under different experimental conditions: The inhi bition of cyclooxygenase by indomethacin, aspirin and aminopyrine was studied under the following three incubation conditions: a) Inhibitors (indomethacin, aspirin and aminopyrine) and arachidonic acid were simultan...

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“…Prostaglandins are synthesised by the gastric mucosa and considered necessary for mucosal protection (Wilson 1996). By direct action on parietal cells, misoprostol inhibits gastric acid secretion, both basally and that stimulated by food, pentagastrin or histamine (Tsai et al 1987). Misoprostol also has a cytoprotective effect on gastric mucosa, although the mechanism is not clear: it is postulated to result from increased production of gastric mucus and bicarbonate, and increased turnover and blood supply of gastric mucosal cells (Tsai et al 1987), which theoretically contributes to ulcer healing.…”

Section: Misoprostolmentioning

confidence: 99%

Gastroprotectants in small animal veterinary practice – a review of the evidence. Part 1: cyto‐protective drugs

Bazelle

Threlfall

Whitley

2018

J of Small Animal Practice

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Diverse drugs with presumed cytoprotective effect have been used therapeutically in small animal veterinary practice for various gastro-intestinal conditions such as oesophagitis, gastric ulceration, gastritis or chronic gastro-enteropathies. Their efficacy has been doubted in human medicine, raising similar questions in the veterinary field. The aim of this review was to assess the current evidence on the efficacy and safety of these drugs in dogs and cats. Through a systematic review of the literature, we identified 37 articles on the use of misoprostol, sucralfate and other gastroprotectants in dogs and cats. There was evidence to support use of misoprostol in the prevention of aspirin-induced gastroduodenal mucosal injury in dogs, and for use of sucralfate in the prevention of acid-induced oesophagitis in cats. However, the overall quality of evidence supporting the use of these drugs in small animal patients was poor. In contrast, there was evidence of important adverse effects, especially drug interaction and gastro-intestinal signs. We therefore recommend prescribing these drugs with caution until further well-conducted studies reveal a useful gastroprotectant effect.

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Effect of misoprostol on histamine-stimulated acid secretion and cyclic AMP formation in isolated canine parietal cells

Cited by 18 publications

References 23 publications

Dual action of prostaglandin E₂ on gastric acid secretion through different EP-receptor subtypes in the rat

Dual action of prostaglandin E₂ on gastric acid secretion through different EP-receptor subtypes in the rat

Different modes of inhibition of rat gastric mucosal 6-keto-PGF1.ALPHA. production by indomethacin, aspirin and aminopyrine.

Gastroprotectants in small animal veterinary practice – a review of the evidence. Part 1: cyto‐protective drugs

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Effect of misoprostol on histamine-stimulated acid secretion and cyclic AMP formation in isolated canine parietal cells

Cited by 18 publications

References 23 publications

Dual action of prostaglandin E2 on gastric acid secretion through different EP-receptor subtypes in the rat

Dual action of prostaglandin E2 on gastric acid secretion through different EP-receptor subtypes in the rat

Different modes of inhibition of rat gastric mucosal 6-keto-PGF1.ALPHA. production by indomethacin, aspirin and aminopyrine.

Gastroprotectants in small animal veterinary practice – a review of the evidence. Part 1: cyto‐protective drugs

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Dual action of prostaglandin E₂ on gastric acid secretion through different EP-receptor subtypes in the rat

Dual action of prostaglandin E₂ on gastric acid secretion through different EP-receptor subtypes in the rat