Orally administered L-arginine and glycine are highly effective against acid reflux esophagitis in rats

Abstract

SummaryBackgroundReflux esophagitis is caused mainly by excessive exposure of the mucosa to gastric contents. In the present study, we examined the effect of several amino acids on acid reflux esophagitis in rats.Material/MethodsAfter 18 h of fasting, acid reflux esophagitis was induced by ligating both the pylorus and the transitional region between the forestomach and the corpus under ether anesthesia, and the animals were killed 4 h later. The severity of esophagitis was reduced by the oral administration of omeprazole, a proton pump inhibitor, or pepstatin, a specific pepsin inhibitor.ResultsThe development of esophageal lesions was dose-dependently prevented by L-arginine and glycine, given intragastrically (i.g.) after the ligation, with complete inhibition obtained at 250 mg/kg and 750 mg/kg, respectively, and these effects were not influenced by the prior s.c. administration of indomethacin or L-NAME. By contrast, both L-alanine and L-glutamine given i.g. after the ligation aggravated these lesions in a dose-dependent manner. These amino acids had no effect on acid secretion but increased the pH of the gastric contents to 1.8~2.3 due to their buffering action.ConclusionsThe results confirmed an essential role for acid and pepsin in the pathogenesis of acid reflux esophagitis in the rat model and further suggested that various amino acids affect the severity of esophagitis in different ways, due to yet unidentified mechanisms; L-alanine and L-glutamine exert a deleterious effect on the esophagitis, while L-arginine and glycine are highly protective, independent of endogenous prostaglandins and nitric oxide.

Ameliorative and antioxidant effects of myrtle berry seed (Myrtus communis) extract during reflux-induced esophagitis in rats

“…In vivo, we firstly showed that ER was accompanied by a decrease in pH and an increase in titratable acidity, which indicates that the used experimental ER model has been successfully established. These results are in line with previous reports (Mahattanadul et al 2011;Nagahama et al 2012). In this experimental model, the gastric acid secreted by parietal cells and pepsin activity in the stomach, but not intestinal alkaline content, are the most important pathogenic factors of ER (Miner 2006;Pawlik et al 2011).…”

A Comparison of Alkaline Water and Mediterranean Diet vs Proton Pump Inhibition for Treatment of Laryngopharyngeal Reflux

“…In a nonacidic environment, exposure of hypopharyngeal cells to pepsin induces the expression of proinflammatory cytokines involved in the inflammation of the esophageal epithelium owing to reflux . In rat models, amino acids, particularly alanine and glutamine, have been shown to aggravate esophagitis by shifting the intraluminal pH to the optimal pH for the proteolytic activity of pepsin . Though discussed extensively as a possible candidate for antagonistic therapy, to date, no therapy has targeted pepsin in the treatment of LPRD or GERD.…”

Activity and MeCP2‐dependent regulation of nNOS levels in enteric neurons

“…Excess nNOS activity is likewise detrimental to GI function; it has been hypothesized that excess NO production underlies postoperative ileus and pseudo‐obstruction, two common functional disorders of GI dysmotility which cause severe clinical morbidity . Additionally, NO is known to play a role in lower esophageal sphincter transient relaxations, the most prominent contributing mechanism to GERD and treatment by nNOS inhibition (NG‐monomethyl‐L‐arginine) reduces acid reflux . Interestingly, GERD is also a prominent GI complaint in RTT …”

“…34,35 Additionally, NO is known to play a role in lower esophageal sphincter transient relaxations, the most prominent contributing mechanism to GERD and treatment by nNOS inhibition (NGmonomethyl-L-arginine) reduces acid reflux. 36,37 Interestingly, GERD is also a prominent GI complaint in RTT. 10 No study has yet determined whether MeCP2-KO mice mirror the GI dysmotility seen in human RTT patients.…”