Adenylate cyclase and H+ production of isolated rat parietal cells in response to glucagon and histamine.

The effect of glucagon and its interaction with histamine on adenylate cyclase (AC), cellular cAMP and [14C]aminopyrine ( [14C]AP) uptake, a reliable index of parietal cell H+ production, was studied in isolated rat gastric cells. AC activation in response to glucagon and histamine correlated with the number of parietal cells. Glucagon (10(-10)-10(-6) mol/l) increasingly stimulated AC (maximal effect: 92% by 10(-7) mol/l) and cellular cAMP (86% by 10(-9) mol/l) of fractions enriched with 80% parietal cells but did not cause a pronounced change of the histamine-stimulated enzyme. If there was any interaction, the effect of both hormones was additive. Glucagon neither changed basal [14C]AP uptake nor interfered with that in response to histamine. The data suggest that if glucagon activates a parietal cell AC this process is not followed by parietal cell H+ production. Furthermore, unlike other inhibitors such as somatostatin or PGE2, glucagon does not reduce acid secretion via the cAMP system of the parietal cell.