Effects of endogenous production and exogenous administration of H2S on gastric acid secretion in rats

Authors

  • Alihosein Saberi
  • Maryam Maleki Physiology Research Center and Dept. Physiology, the school of Medicine, Ahvaz Jundi Shapur University of Medical Sciences, Ahvaz, Iran
  • Mohammad Kazem Gharib Naseri Physiology Research Center and Dept. Physiology, the school of Medicine, Ahvaz Jundi Shapur University of Medical Sciences, Ahvaz, Iran
  • seyyed Ali Mard Physiology Research Center and Dept. Physiology, the school of Medicine, Ahvaz Jundi Shapur University of Medical Sciences, Ahvaz, Iran
Abstract:

Introduction: Recently, hydrogen sulfide has been introduced as the third gas that acts as a transmitter. It has many physiological and pharmacological roles in the human body. The aim of the present study was to investigate the effect of exogenously administered and endogenously produced H2S on the basal and distention-induced gastric acid secretion in rats. Methods: Forty-nine male Wistar rats (150-200 g) were randomly assigned into 7 groups (7 rats per group). To evaluate the effect of H2S on the basal acid secretion, three groups of animals received an IV bolus of NaHS, a H2S donor, at the doses of 20, 40 or 80 μg/Kg. The effects of IV NaHS 20, 40 or 80 μg/Kg were also investigated on distention-induced gastric acid secretion in other three groups. In order to evaluate the effect of endogenously produced H2S on distention-induced gastric acid secretion, one group of animals received IV propargylglycine (PAG), a cystathionine-γ-lyase inhibitor, 100 mg/kg. Results: NaHS decreased the basal and distention-induced gastric acid secretion in a dose-dependent manner (P<0.01). PAG increased the gastric output in response to distention compared to the control group (P<0.001). Conclusion: Our results showed that both exogenous administration and endogenous production of H2S decrease the gastric acid output. Also, the findings of the present study suggest that endogenously produced H2S has a modulatory effect on stimulated gastric acid output similar to nitric oxide (NO).

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Journal title

volume 15  issue None

pages  499- 506

publication date 2012-01

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