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Gastric Cyclic Nucleotide Concentration in Health and Disease

1977; Elsevier BV; Volume: 73; Issue: 4 Linguagem: Inglês

10.1016/s0016-5085(19)31775-5

1528-0012

Robert A. Levine, E.H. Schwartzel, S. Bachman, John N. Talev,

Neuroendocrine Tumor Research Advances

Cyclic AMP and cyclic GMP concentrations were measured in suction biopsy specimens of gastric fundic and antral mucosa and in gastric juice in response to maximum stimulation by histamine (0.015 mg per kg per hr), betazole (1.5 mg per kg), and pentagastrin (6 μg per kg) in 14 normogastrinemic healthy subjects, in 46 patients with dyspepsia or peptic ulcer (PU) disease and normal serum gastrin levels, and in 14 patients with hypergastrinemia, including 8 with pernicious anemia (PA), 3 with Zollinger-Ellison (ZE) disease, and 3 with gastric carcinoma. No regional differences were noted in unstimulated gastric antral or fundic cyclic nucleotide content in normal subjects or patients. During secretagogue stimulation no significant changes in cyclic nucleotide concentrations were observed in antral or fundic mucosa of healthy subjects or patients. During basal hourly secretion, cyclic nucleotide concentration and output in gastric juice was relatively constant, suggesting a steady state of secretion. After secretagogue stimulation, the concentrations of cyclic AMP and cyclic GMP were reduced by at least 50% and correlated with the increased parietal volume output, suggesting a dilutional effect. There was no significant change in gastric juice cyclic nucleotide output except in PU subjects after betazole stimulation, in whom cyclic AMP production increased almost 2-fold. This change in gastric juice cyclic AMP appeared proportional to a greater parietal volume flow and did not reflect intracellular mucosal events. Similarly, a decreased concentration of cyclic AMP in the basal and stimulated gastric juice of ZE patients and a reduced cyclic AMP output in PA patients also appeared proportional to volume flow. The presence of cyclic AMP in unstimulated gastric juice in PA suggested, in part, a nonparietal origin for cyclic AMP, probably derived from interstitial fluid secretion or transmucosal exudation from plasma. It is concluded that intra- or extracellular gastric cyclic AMP or cyclic GMP concentrations are not modulated by secretagogue stimulation, circulating high gastrin levels, alteration in intraluminal pH, or increasing age. These studies fail to implicate cyclic nucleotides as intracellular mediators of stimulated gastric acid secretion in healthy subjects, PU disease PA, ZE disease or gastric carcinoma.