Abstract
The ECL cells are histamine- and pancreastatin-secreting endocrine cells in the oxyntic mucosa, thought to release a blood Ca 2+-lowering peptide hormone upon stimulation by gastrin. Previously, we have shown that the ECL cells do not respond to perturbations in blood Ca 2+. In the present study, we examine if Ca 2+ in the gastric lumen will affect the activity of the gastrin-ECL-cell axis. Freely fed or food deprived (48 h) rats were given an oral load of CaCl 2 (or NaCl), and the blood Ca 2+ concentration was monitored. The serum gastrin concentration at sacrifice, 3 h after ingestion of CaCl 2, was measured together with two parameters of ECL cell activity: the oxyntic mucosal histidine decarboxylase (HDC) activity and the serum pancreastatin concentration. The circulating concentrations of calcitonin and parathyroid hormone (PTH) were also measured. Oral CaCl 2 raised the blood Ca 2+ in a dose-dependent manner. The two highest doses (which caused damage to the oxyntic mucosa) raised the serum gastrin concentration and the HDC activity in both fed and fasted rats; the serum pancreastatin concentration remained unaffected. Oral CaCl 2 raised the serum calcitonin concentration and lowered the serum PTH concentration. The effects of high doses of oral CaCl 2 on the serum gastrin concentration and on the oxyntic mucosal HDC activity could be reproduced by a high dose of NaCl. Thus the effects are probably not due to Ca 2+ per se. We conclude that the gastrin-ECL-cell axis in the rat does not respond to peroral Ca 2+. Since the ECL cells do not respond to either circulating or peroral Ca 2+ they are unlikely to secrete a calciotropic hormone.
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