Interactions between signalling pathways such as the cyclic AMP and the Ca2+/phosphatidylinositol pathway may occur and be of major relevance in the regulation of cell function. We demonstrate here that cyclic-AMP-dependent mechanisms cause a marked increase in frequency and peak free Ca2+ of alpha 1-receptor-induced Ca2+ transients in single hepatocytes and lower the threshold for alpha 1-receptor agonists. Adrenaline at low physiological concentrations generates alpha 1-receptor-induced Ca2+ transients, which requires activation of the beta 2-receptor signalling pathway. We conclude that an interaction between the alpha 1-receptor signalling pathway and cyclic-AMP-dependent mechanisms activated by beta 2-receptor occupation is crucial to elicit a complete adrenergic response to adrenaline at physiological concentrations in rat hepatocytes.