Isolated, lumen-perfused, whole stomach preparations from mouse and immature rat produced a stable basal acid output which, although not blocked by histamine H2-, acetylcholine M- or CCKB/gastrin receptor antagonists, was almostly completely blocked by the H+/K(+)-ATPase inhibitor, omeprazole, and the metabolic inhibitor, sodium thiocyanate (NaSCN). 2. Fully-defined concentration-effect curves could be obtained on both assays with the phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX) and with dibutyryl cyclic AMP. 3. On the rat stomach assay, histamine H2-receptor blockade had no effect on the IBMX curve. In contrast, the IBMX response in the mouse was abolished by histamine H2-receptor blockade. On both assays responses to dibutyryl cyclic AMP were resistant to H2-receptor blockade. 4. In the absence of suprathreshold endogenous histamine, it is argued that H+/K(+)-ATPase mediated basal acid secretion from the mouse stomach assay is regulated by something other than cyclic AMP.
