Indomethacin enhances histamine-stimulated acid production in rabbit isolated fundic glands

Schwartzel, Edmund H.; Levine, Robert A.; Schwartz, Solomon; Ganley, Carolyn

doi:10.1016/0262-1746(84)90121-5

Cited by 15 publications

(15 citation statements)

References 13 publications

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“…These results contrast with those previously reported by Murthy and Levine (37) and Levine et al (27), showing that acetylsalicylic acid (10 M) and indomethacin (1-100 M) reinforced the rate of acid formation in isolated parietal cells treated with 100 M histamine by ϳ50-100%. On the other hand, Schwartzel et al (48) observed that, in isolated rabbit gastric glands, indomethacin (100 M) increased the rate of aminopyrine uptake stimulated by histamine (1-100 M) by approximately threefold. We have no clear explanation for the less-marked NSAID reinforcement of histamine-mediated acid secretion observed by us.…”

Section: Effects Of Nsaids On the Cellular Integrity Of The Isolated mentioning

confidence: 96%

“…The biochemical mechanism of this potentiation is not well established. However, it appears to be dependent on the presence of Ca 2ϩ in the incubation medium and occurs without significant changes in either cAMP or inositol 1,4,5-trisphosphate levels or in H ϩ -K ϩ -ATPase activity (27,48).…”

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confidence: 96%

“…Different in vivo studies carried out in humans have demonstrated that both acetylsalicylic acid and indomethacin are able to increase the basal rate of acid formation (8,12,21,29) and to potentiate acid secretion stimulated by histamine (21,29). Furthermore, in vitro studies carried out in isolated rabbit fundic glands (48), in preparations of rat gastric mucosa (41), or in isolated rabbit parietal cells (27,28,37) have demonstrated that micromolar concentrations of aspirin and other NSAIDs, like indomethacin, piroxicam, and naproxen, may potentiate gastric acid secretion stimulated by histamine, dibutyryl cAMP, or forskolin without affecting the basal rate of acid formation. The biochemical mechanism of this potentiation is not well established.…”

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confidence: 97%

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Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Salvatella¹,

Rossi²,

Valle³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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In nonstimulated rabbit gastric glands, acetylsalicylic acid (10-500 microM) and indomethacin (3-300 microM) did not significantly modify the basal rate of acid secretion, whereas diclofenac and piroxicam (10-1,000 microM each) caused a marked and dose-dependent inhibitory effect (EC(50) = 138 and 280 microM, respectively). In gastric glands stimulated by histamine (100 microM), diclofenac also reduced the rate of acid formation in a dose-dependent manner. In contrast, acetylsalicylic acid, indomethacin, and piroxicam exerted a biphasic effect; thus low concentrations (3-100 microM) of these three agents significantly increased the rate of histamine-stimulated acid secretion (10-20% over the corresponding control value) by a cAMP-independent mechanism, whereas higher concentrations reduced the rate of acid formation. With respect to underlying biochemical mechanisms that could mediate inhibitory effects of NSAIDs on gastric acid formation, it was observed that both diclofenac and piroxicam, but not acetylsalicylic acid or indomethacin, decreased the glandular content of ATP, inhibited hydrolytic activity of gastric gland microsomal H(+)-K(+)-ATPase, and reduced the rate of H(+)-K(+)-ATPase-dependent proton transport across microsomal membranes in a dose-dependent manner. Furthermore, diclofenac and piroxicam also significantly increased passive permeability of microsomal membranes to protons. In conclusion, our work shows that diclofenac and piroxicam cause a significant reduction in the rate of basal and histamine-stimulated acid formation in isolated rabbit gastric glands at concentrations that can be attained in the gastric lumen of patients treated with these drugs. Mechanisms involved in these inhibitory effects appear to be multifocal and include different steps of stimulus-secretion coupling.

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Section: Effects Of Nsaids On the Cellular Integrity Of The Isolated mentioning

confidence: 96%

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confidence: 96%

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confidence: 97%

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Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Salvatella¹,

Rossi²,

Valle³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…IC50 of Garcinia kola Heckel seed extract is 43.8 g/ml while IC50 of omeprazole, a conventional inhibitor, is 32.3 g/ml (Onasanwo et al, 2011). Second, histamine stimulates acid secretion while NSAIDs enhance the effect of histamine on acid secretion (Schwartzel et al, 1984;Shamburek and Schubert., 1992). Studies have demonstrated that oral administration of the extract of Trichosanthes cucumerina (aerial parts) was more effective then chlorpheniramine in reduction of wheal size induced by subcutaneous injection of histamine, suggesting antihistamine effect (Arawwawala et al, 2010).…”

Section: B Inhibition Of Acid Secretionmentioning

confidence: 99%

Anti-Ulcerogenic Efficacy and Mechanisms of Edible and Natural Ingredients in Nsaid-Induced Animal Models

Man

2017

Afr J Tradit Complement Altern Med

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Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are a class of the most commonly used medicines and proven to be effective for certain disorders. Some people use NSAIDs on daily basis for preventive purpose. But a variety of severe side effects can be induced by NSAIDs. Studies have shown that edible natural ingredients exhibit preventive benefit of gastric ulcer. This paper reviews the efficacy and safety of edible natural ingredients in preventing the development of gastric ulcer induced by NSAIDs in animal models. Methods: A systematic literature search was conducted on PubMed, using the terms "herbal medicines" and "gastric ulcer", "herbal medicines" and "peptic ulcer", "food" and "peptic ulcer", "food" and "gastric ulcer", "natural ingredient" and "peptic ulcer", "natural ingredient" and "gastric ulcer", "alternative medicine" and "peptic ulcer", "alternative medicine" and "gastric ulcer", "complementary medicine" and "peptic ulcer", "complementary medicine" and "gastric ulcer" in papers published in English between January 1, 1960 and January 31, 2016, resulting in a total of 6146 articles containing these terms. After exclusion of studies not related prevention, not in NSAID model or using non-edible natural ingredients, 54 articles were included in this review.Results: Numerous studies have demonstrated that edible natural ingredients exhibit antiulcerogenic benefit in NSAIDinduced animal models. The mechanisms by which edible, ingredient-induced anti-ulcerogenic effects include stimulation of mucous cell proliferation, antioxidation, inhibition of gastric acid secretion, as well as inhibition of H(+), K(+)-ATPase activities. Utilization of edible, natural ingredients could be a safe, valuable alternative to prevent the development of NSAID-induced gastric ulcer, particularly for the subjects who are long-term users of NSAIDs.

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“…to histamine, which in some studies was found to be enhanced by indomethacin and not affected in others [4][5][6]. Recently a release of PGs by histamine has been observed in rats and the cytoprotective action of histamine in this species was ascribed to this effect [7].…”

Section: Introductionmentioning

confidence: 97%

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

et al. 1990

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The interference between histamine and endogenous prostaglandins (PGs) was investigated in the isolated gastric fundus from immature rats by evaluating the effect of nonsteroidal antiinflammatory agents (NSAIDs) on the acid response to histamine and the effect of histamine on PGs production by the gastric mucosa. Indomethacin (10(-5) M) and diclofenac (10(-5) M) caused a dose-dependent enhancement of the response to histamine, dimaprit and DBcAMP, but did not affect bethanechol-, isoprenaline- and forskolin-induced acid production. The enhancing effect of indomethacin was abolished in low Ca2+ medium. PGE2 and 6-keto PGF1 alpha levels in the mucosal solution were not modified by histamine, while being reduced by indomethacin. From these data it is concluded that endogenous PGs may negatively modulate the secretory response to histamine. However, a direct effect of the amine on cyclooxygenase to increase PGs synthesis seems to be excluded since histamine did not modify PGs levels in the mucosal solution.

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Indomethacin enhances histamine-stimulated acid production in rabbit isolated fundic glands

Cited by 15 publications

References 13 publications

Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Anti-Ulcerogenic Efficacy and Mechanisms of Edible and Natural Ingredients in Nsaid-Induced Animal Models

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

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