Antisecretory effect of hydrogen sulfide on gastric acid secretion and the involvement of nitric oxide.
The present study was designed to investigate the effect of H2S on distention-induced gastric acid secretion. Fifty-two rats were randomly assigned to seven experimental groups. The gastric acid secretion was stimulated by gastric distention. Two groups of rats received L-cysteine or saline for 5 days before stimulation of the gastric acid secretion. Two groups of animals also received NaHS or saline just prior to stimulation of the gastric acid secretion. The effect of L-NAME and propargylglycine was also investigated. The mucosal levels of the gene expression of cyclooxygenase-2 (COX-2), endothelial nitric oxide synthase (eNOS), and H(+)/K(+)-ATPase α-subunit were quantified by qPCR and luminal concentrations of NO were determined. NaHS and L-cysteine decreased the gastric acid output in response to distention. The mRNA expression of H(+)/K(+)-ATPase α-subunit decreased by NaHS and L-cysteine as compared with the control group while gene expression of eNOS and COX-2 was upregulated. The inhibitory effect of NaHS on distention-induced gastric acid secretion was mitigated by pretreatment of L-NAME. These findings suggest the involvement of NO in mediating the antisecretory effect of H2S.
Research Institute for Infectious Diseases of Digestive System, Physiology Research Center (PRC) and Department of Physiology, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357 15794, Iran.
Seyyed Ali
SA
Mard
Department of Physiology, The School of Medicine, Tehran University of Medical Sciences, Tehran, Iran ; Research Institute for Infectious Diseases of Digestive System, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357 15794, Iran.
Hasan
H
Askari
Research Institute for Infectious Diseases of Digestive System and Department of Virology, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357 15794, Iran.
Niloofar
N
Neisi
Research Institute for Infectious Diseases of Digestive System, Physiology Research Center (PRC) and Department of Physiology, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357 15794, Iran.
Ali
A
Veisi
D000480:Alkynes / Q000494:pharmacology; D000818:Animals; D051546:Cyclooxygenase 2 / Q000378:metabolism; D003545:Cysteine / Q000378:metabolism; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism*; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D017506:H(+)-K(+)-Exchanging ATPase / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013440:Sulfides / Q000494:pharmacology
D000480:Alkynes; D013440:Sulfides; D009569:Nitric Oxide; C009055:propargylglycine; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D051546:Cyclooxygenase 2; D017506:H(+)-K(+)-Exchanging ATPase; C025451:sodium bisulfide; D003545:Cysteine; D005998:Glycine; D019331:NG-Nitroarginine Methyl Ester; D006862:Hydrogen Sulfide