Role of Dopamine in Control of Duodenal Mucosal Bicarbonate Secretion
The bicarbonate secretion of the duodenal mucosa alkalinizes the viscoelastic mucus gel adherent to the mucosal surface and is one major mechanism in the protection of this epithelium against luminal acid (and pepsin). The secretion is influenced by stimulatory and inhibitory neural impulses and by local mucosal production of prostaglandins and other substances (Flemstrom 1993), and is deficient in patients with chronic and acute duodenal ulcer disease (Isenberg et al. 1987, Mertz-Nielsen et al. 1993). Recent reports have indicated that some dopaminergic compounds are efficacious in the treatment of duodenal ulcer disease in humans (Sikriric et al. 1991), and protective effects of such compounds have been observed in animal models of ulcer disease (Glavin 1989, MacNaughton & Wallace 1989, Glavin & Szabo 1990, Aho & Lindén 1992). It is also well known that dopamine receptor agonists affect the motility in several segments of the gastrointestinal tract and effects on salivary gland and pancreatic exocrine secretions and on small intestinal NaCl absorption have been reported (Donowitz et al. 1982, Willems et al. 1985). These findings made it of interest to investigate the effects of dopamine and some dopaminergic compounds on the duodenal mucosal bicarbonate secretion. The secretion was studied in anaesthetized rats and in human volunteers. Duodenal mucosal production of cyclic AMP was measured in isolated duodenal villus and crypt enterocytes.
KeywordsDopamine Bicarbonate Prostaglandin Luminal Catecholamine
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