THE ROLE OF GASTRIC MUCOSAL HISTAMINE AND HISTIDINEDECARBOXYLASE ACTIVITY IN MECHANISMS RELATED TO ACID SECRETION IN RATS

Abstract

Gastric mucosal histamine and histidinedecarboxylase activitiy stimulated by tetragastrin was studied biochemically in rats in order to determine the direct pathway from gastrin to histaminocyte, in cases of gastric acid secretion in vivo. Gastric mucosal histamine was decreased by injection of tetragastrin while histidinedecarboxylase activity was significantly increased, and secretin suppressed the histidinedecarboxylase activity stimulated by tetragastrin. These results suggest that gastrin acts directly and specifically on histaminocytes.
The levels of serum gastrin, mucosal histamine and histidinedecarboxylase activity showed significant increases in the presense of cimetidine and these increments were not suppressed after abolishment of secondary increases in endogenous gastrin secretion by intragastric perfusin with hydrochloric acid. Therefore, cimetidine acts indirectly on histaminocytes through gastrin producing cells.
Gastric acid secretion stimulated by tetragastrin was also inhibited by cimetidine, and was completely inhibited by cimetidine plus α-Fluoromethylhistidine, a specific inhibitor of histidinedecarboxylase. These results suggest that increments in histidinedecarboxylase activity induced by cimetidine relate to gastric acid secretion.
The important role of histamine in the mechanism of gastric acid secretion was thus elucidated.