Research article

Nitric oxide-an endogenous inhibitor of gastric acid secretion in isolated human gastric glands

Anna Berg¹ , Stefan Redeen² , Ann-Charlott Ericson¹ and Sven Erik Sjöstrand¹

¹Department of Biomedicine and Surgery, Division of Cell Biology, Linköping University, Linköping, Sweden

²Surgery Department, University Hospital, Linköping, Sweden

author email corresponding author email

BMC Gastroenterology 2004, 4:16doi:10.1186/1471-230X-4-16

Published:	6 August 2004

Abstract

Background

Endothelial nitric oxide synthase (eNOS) has previously been detected in the glandular part of the human gastric mucosa. Furthermore, nitric oxide (NO) has been shown to influence gastric secretion in various animal models. The present study was conducted to investigate the influence of exogenously and endogenously derived NO on histamine- and cAMP-stimulated gastric acid secretion in isolated human oxyntic glands.

Methods

Oxyntic glands were isolated from human gastric biopsies and were subsequently pre-treated with NO donors and nitric oxide synthase inhibitors and then exposed to histamine or dibutyryl-cAMP (db-cAMP). The secretory response of the glands was determined as accumulation of [¹⁴C]aminopyrine.

Results

The histamine- or db-cAMP-induced acid secretion was attenuated by L-arginine, a known source of endogenous NO, and also by the NO-donors sodium nitroprusside (SNP) and S-nitroso-N-acetyl-penicillamine (SNAP). Pre-treatment with either of the NOS inhibitors N^G-nitro-L-arginine methyl ester (L-NAME) or N^G-nitro-L-arginine (L-NNA) enhanced the secretory response.

Conclusion

Our results show that NO inhibits gastric acid secretion in isolated human gastric glands, and that there is endogenous formation of NO within the glandular epithelium in the vicinity of the parietal cells.