This review has focused on the properties of the ATP-sensitive K-channel found in cardiac and skeletal muscle, and in pancreatic beta-cells. It is conceivable that this channel will be found in other cell types. In particular, it would be worthwhile looking for its presence in those cells in which electrical activity is linked to metabolism, glucose concentration, or oxygen levels. Obvious examples are the glucoreceptor neurons of mammalian brain and chemoreceptors such as those of the carotid body. While ATP-sensitive K-channels in cardiac and skeletal muscle membranes are rather similar, there are a few significant differences between these channels and that found in the beta-cell. Most notably, the latter is more sensitive to inhibition by ATP and sulphonylureas. It remains to be seen whether they also differ in the ability of nucleotides to activate the channel. Considerable confusion also still surrounds the physiological regulation of the ATP-sensitive K-channel in intact cells. Although the general consensus seems to be that [ATP]i modulates channel activity, the role of other nucleotides and ions as well as the way in which their concentrations alter with metabolism requires further elucidation. A combined electrophysiological and biochemical approach is likely to prove most successful in establishing which second messenger systems contribute to the physiological regulation of the ATP-sensitive K-channel. Finally, the close correlation between cell metabolism and the activity of the ATP-sensitive K-channel raises the intriguing possibility that disorders of cell metabolism might produce alterations in channel activity and consequent changes in cell function.