Dual inhibitory actions of somatostatin on isolated gastric glands

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Abstract
The growth hormone release‐inhibiting hormone or somatostatin is a potent inhibitor of gastric acid secretion. In the present paper these inhibiting properties were tested on isolated gastric glands from rabbit fundic mucosae, prepared as according to Berglindh & ÖBRINK (1976). Parietal cell activity was measured as [14C]aminopyrine (AP) accumulation and O2‐consumption. Glandular histamine release was determined after condensation with o‐phthalaldehyde and measured fluorometrically. In the gastric glands there are two possible main processes that can be inhibited, namely (1) the release of histamine from some endocrine cells and (2) the activity of the parietal cell itself. It was found that somatostatin acted on both mechanisms. Basal histamine release was, however, not affected by somatostatin while the release induced by pentagastrin (Pg) at a concentration of 3 times 10‐9M, or acetylcholine (10‐5M) was dose‐dependently (10‐12to 10‐6M) inhibited by this peptide. Maximal inhibition, which was about 70%, occurred at a dose of 10‐8M somatostatin. Somatostatin also depressed parietal cell activity induced by histamine (10‐6to 10‐4M), isobutyl‐methyl‐xanthine (IMX, 10‐5to 10‐4M) or the combination of IMX (10‐5M) and Pg (3 times 10‐9M) Basal parietal cell activity was, however, unaffected. The IMX (10‐4M) induced parietal cell activity in cimetidine‐treated (10‐4M) glands was also depressed by somatostatin, which indicates an action directly on the parietal cell not mediated via H2‐receptors. The dual inhibitory actions of somatostatin are probably not mediated via stimulation of prostaglandin synthesis since indomethacin (3 times 10‐6M) did not diminish its effects.

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