Summary
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1.
The effects of gastrin I, bethanechol, histamine and reserpine on gastric acid secretion and the expiration of radioactive carbon dioxide have been studied in anaesthetized carboxyl-14C-l-histidine-loaded rats.
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2.
All compounds tested stimulated gastric acid secretion. In unstimulated animals the radioactive carbon dioxide in the expired air dropped exponentially with time; it was increased by reserpine and histamine, but not by gastrin and bethanechol.
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3.
In gastrin- and histamine-treated animals acetazolamide suppressed gastric acid secretion as well as the expiration of radioactive carbon dioxide.
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4.
The effect of histamine on the expiration of radioactive carbon dioxide can be attributed to effects other than the enhanced decarboxylation of histidine. The response to reserpine can be explained as an activation of histidine decarboxylase. Whether the failure of gastrin I and bethanechol to increase the expiration of radioactive carbon dioxide documents their inability to stimulate histidine decarboxylase in vivo, cannot be decided.
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This work was supported by a grant from the Deutsche Forschungsgemein-schaft and the Universitätsbund Tübingen.
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Albinus, M., Sewing, K.F. Gastric acid secretion and the expiration of radioactive carbon dioxide of carboxyl-14C-labelled histidine-loaded rats. Naunyn-Schmiedebergs Arch. Pharmak. 271, 149–156 (1971). https://doi.org/10.1007/BF00998576
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DOI: https://doi.org/10.1007/BF00998576