Effect of L-dopa with and without inhibition of extra cerebral dopa decarboxylase on gastric acid secretion and gastrin release in man.
The present study was undertaken to investigate the possibility that central nervous system monoaminergic pathways may play a role in the control of gastric acid and gastrin secretion in man. Submaximal pentagastrin stimulated (0.25 micrograms/kg/h) gastric acid secretion, as well as basal gastrin concentrations were studied in two groups of subjects. The first group received oral administration of placebo and the catecholamine precursor L-dopa (500 mg); the second group was treated with placebo and the association of L-dopa (100 mg) plus carbidopa (35 mg) after pretreatment with carbidopa (50 mg every six hours for four doses), a schedule which is known to increase brain catecholamine concentrations. In comparison with placebo, stimulated gastric acid secretion was reduced by L-dopa alone, whereas was not modified by L-dopa plus carbidopa. Basal gastrin concentrations were increased after L-dopa and after L-dopa plus carbidopa. These data show that basal gastrin concentration is raised by central catecholamine augmentation; but gastric acid secretion seems to be influenced by changes of peripheral catecholamine concentrations. It is suggested that dopamine and perhaps noradrenaline, but not adrenaline, are important in these effects.
D000328:Adult; D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D002230:Carbidopa / Q000494:pharmacology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000097:blood*; D006801:Humans; D007980:Levodopa / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D010418:Pentagastrin / Q000494:pharmacology
D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D005755:Gastrins; D007980:Levodopa; D010418:Pentagastrin; D002230:Carbidopa