This review of the past year's literature focuses on progress in the elucidation of the pathways and mechanisms controlling gastric acid secretion at the central, peripheral, and intracellular levels. Injection of thyrotropin-releasing peptide and neuropeptide Y into the central nervous system stimulates acid secretion; the effects are mediated via the vagus nerve. Elevated intracranial pressure and increasing age also stimulate acid secretion, whereas γ-aminobutyric acid, tachykinins, and prostaglandins act centrally to inhibit acid secretion. The stimulatory effect of gastrin and acetylcholine on acid secretion may be mediated via release of histamine, possibly from enterochromaffin-like cells. Histamine stimulation of the parietal cell is accompanied by increasing cellular levels of cyclic AMP and dephosphorylation of type II cyclic AMP-dependent protein kinase. Besides releasing histamine, muscarinic agonists appear to stimulate the parietal cell directly via the M3-receptor subtype. This subtype is also coupled to release of intracellular calcium and influx of extracellular calcium. Glucagon-like peptide, low concentrations of ethanol, cigarettes, and coffee stimulate acid secretion whereas neurotensin, oxyntomodulin, serotonin, interleukins, and high concentrations of ethanol inhibit acid secretion. Vasoactive intestinal polypeptide exerts dual stimulatory and inhibitory actions on acid secretion; the inhibitory effect is mediated by release of somatostatin. Candidate enterogastrones include secretin, cholecystokinin, somatostatin, and possibly peptide YY.