The role of dopamine in the formation of gastric ulcers in rats

Sikirić, Predrag; Geber, Juraj; Suchanek, Ernest; Ivanović, Drago; Gjuriš, V.; Aleksić, J.; Reić, Petar; Marović, Anton

doi:10.1016/0014-2999(85)90249-3

Cited by 33 publications

(15 citation statements)

References 3 publications

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“…Our results also support the clinical effectiveness of sulpiride reported in the patients of peptic ulcer disease [12,16,17,28] and the doses used by us are relevant to clinical situations when extrapolated to man on the basis of the surface areas of the two species [29]. However, these observations are contradictory to the ulcer aggravating activity of sulpiride reported by Sikiric et al [5] but it may be noted that they had used much smaller dose of sulpiride (0.001-0.50 mg/kg) in their study. Sulpiride has shown differential dose and model-specific effects in other studies too [30].…”

Section: Discussionsupporting

confidence: 89%

“…In recent years dopamine has been implicated in the genesis of experimentally induced gastric and duodenal ulcers [1][2][3][4][5]. Clinically too, a high incidence of duodenal ulcers has been observed in patients with Parkinson's disease (associated with dopamine deficiency) and a low occurrence is seen in schizophrenics (associated with dopamine excess or hyperactivity) [6,7].…”

Section: Introductionmentioning

confidence: 99%

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Gastric and duodenal anti-ulcer activity of sulpiride, a dopamine D2 receptor antagonist, in rats

Desai

Parmar

1994

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The gastric and duodenal anti-ulcer activity of sulpiride, a dopamine D2 receptor antagonist, was studied on various types of experimentally induced ulcers in rats, viz., pylorus ligation and water immersion + restraint stress-induced gastric ulcers, gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs and reserpine, and duodenal ulcers induced by cysteamine hydrochloride. It has been found to possess significant anti-ulcer activity against all these models. In 19 h pylorus ligated rats, it significantly reduced the gastric secretion, increased the fucose and sialic acid concentration of the gastric juice and reduced its protein content, thus increasing the total carbohydrate:protein (TC/PR) ratio. These results suggest that the antisecretory and gastric mucosal barrier strengthening effects of sulpiride may be responsible for its anti-ulcer activity. A central component also appears to be involved in its anti-ulcer action against water immersion + restraint stress model. The results of this study provide a rationale for its beneficial effect seen in the therapy of peptic ulcer disease.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Gastric and duodenal anti-ulcer activity of sulpiride, a dopamine D2 receptor antagonist, in rats

Desai

Parmar

1994

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“…These results suggest that dopamine does not have any deleterious infl uence on the healing of gastric ulcers. Dopamine and its agonist have a protective action against various lesion models in the stomach and duodenum (Lauterbach et al, 1977;Szabo et al, 1987;Hernadez et al, 1984;Sikiric et al, 1985). Szabo et al (1987) demonstrated a causal relationship between a decrease in dopamine levels and the occurrence of duodenal ulcers in cysteamine-treated rats and suggested an important role of endogenous dopamine in the duodenal mucosa defense.…”

Section: Discussionmentioning

confidence: 99%

Effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats

2007

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Dopamine, as a neurotransmitter in the brain, is also present in the gastroduodenal mucosa and has been implicated in several functions in these tissues. Recent study showed that dopamine acts as a potent antitumor/angiogenic activity through suppression of growth factor expression. Since growth factors are known to play a crucial role in the mechanism of wound healing, it is possible that dopamine has a deleterious influence on the healing of gastric ulcers. In the present study, we examined the effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats. Gastric ulcers were induced in male SD rats by serosal application of acetic acid for 60 sec. Dopamine was subcutaneously given twice daily for 7 days, starting 3 days after ulceration. In some case, the osmotic mini-pump filled with dopamine was implanted into the dorsal subcutaneous space in rats for 7 days. VEGF and Flk-1 mRNA expressions were determined by RT-PCR. Dopamine (3, 10 and 30 mg/kg) given subcutaneously for 7 days did not significantly affect the healing of gastric ulcers. The expression of VEGF and Flk-1 mRNA in the ulcerated mucosa was up-regulated after ulceration, and these expressions were not affected by dopamine. Likewise, dopamine (0.6 mg/kg/hr) infused continuously using the osmotic mini-pump also had no effect on the healing of these ulcers. These results suggest that dopamine, although reportedly shows a potent antitumor/angiogenic activity, does not cause any influence on the healing of the pre-existing gastric ulcers in rats.

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“…For example, deregulated intestinal motility may lead to lesion induction, and, eventually, to ulcer development, which may predispose to inflammation. In this context, dopamine or its agonists have been reported to act as protective agents in various rat ulcer models (100, 101). More recently, it was shown that dopamine acts via DAR2 to suppress both increased motility and ulcer development induced by chemical insult (102).…”

Section: Dopamine and Mucosal Immunity In Inflammatory Bowel Diseasesmentioning

confidence: 99%

The Dopaminergic System in Autoimmune Diseases

2014

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Bidirectional interactions between the immune and the nervous systems are of considerable interest both for deciphering their functioning and for designing novel therapeutic strategies. The past decade has brought a burst of insights into the molecular mechanisms involved in neuroimmune communications mediated by dopamine. Studies of dendritic cells (DCs) revealed that they express the whole machinery to synthesize and store dopamine, which may act in an autocrine manner to stimulate dopamine receptors (DARs). Depending on specific DARs stimulated on DCs and T cells, dopamine may differentially favor CD4+ T cell differentiation into Th1 or Th17 inflammatory cells. Regulatory T cells can also release high amounts of dopamine that acts in an autocrine DAR-mediated manner to inhibit their suppressive activity. These dopaminergic regulations could represent a driving force during autoimmunity. Indeed, dopamine levels are altered in the brain of mouse models of multiple sclerosis (MS) and lupus, and in inflamed tissues of patients with inflammatory bowel diseases or rheumatoid arthritis (RA). The distorted expression of DARs in peripheral lymphocytes of lupus and MS patients also supports the importance of dopaminergic regulations in autoimmunity. Moreover, dopamine analogs had beneficial therapeutic effects in animal models, and in patients with lupus or RA. We propose models that may underlie key roles of dopamine and its receptors in autoimmune diseases.

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The role of dopamine in the formation of gastric ulcers in rats

Cited by 33 publications

References 3 publications

Gastric and duodenal anti-ulcer activity of sulpiride, a dopamine D2 receptor antagonist, in rats

Gastric and duodenal anti-ulcer activity of sulpiride, a dopamine D2 receptor antagonist, in rats

Effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats

The Dopaminergic System in Autoimmune Diseases

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