Figure 2.

Accumulation of ¹⁴C-labeled aminopyrine in histamine-stimulated gastric glands. All values are expressed as percent of the gastric acid secretion induced by histamine (considered to be 100%), which was calculated separately for gastric glands isolated from each of the healthy volunteers. Each symbol represents the results for one individual. a) Accumulation of ¹⁴C-aminopyrine in glands pretreated with the NO donor sodium nitroprusside (SNP, 1 mmol/L) or with L-arginine (0.1 mmol/L), the substrate for endogenous NO production. It can be seen that SNP markedly reduced AP accumulation (median = 48%; p < 0.05), which indicates that NO inhibits acid secretion from the isolated glands. Background ¹⁴C-aminopyrine accumulation (bg) is also shown. b) Accumulation of ¹⁴C-aminopyrine in gastric glands pretreated with the NOS inhibitors L-NNA (0.1 mmol/L) and L-NAME (1 mmol/L), respectively. L-NAME caused increased accumulation (median = 147%; p < 0.05), which suggests that acid secretion is elevated when endogenous NO production is prevented, indicating an inhibitory role for endogenous NO in human gastric glands. D-NAME, which is the biologically inactive stereo isomer of L-NAME, did not have an effect on acid secretion, and it was therefore used as a control substance.