Evidence that peroral calcium does not activate the gastrin-ECL-cell axis in the rat.

The ECL cells are histamine- and pancreastatin-secreting endocrine cells in the oxyntic mucosa, thought to release a blood Ca2+-lowering peptide hormone upon stimulation by gastrin. Previously, we have shown that the ECL cells do not respond to perturbations in blood Ca2+. In the present study, we examine if Ca2+ 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 CaCl2 (or NaCl), and the blood Ca2+ concentration was monitored. The serum gastrin concentration at sacrifice, 3 h after ingestion of CaCl2, 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 CaCl2 raised the blood Ca2+ 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 CaCl2 raised the serum calcitonin concentration and lowered the serum PTH concentration. The effects of high doses of oral CaCl2 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 Ca2+ per se. We conclude that the gastrin-ECL-cell axis in the rat does not respond to peroral Ca2+. Since the ECL cells do not respond to either circulating or peroral Ca2+ they are unlikely to secrete a calciotropic hormone.