title: Messenger-mediated control of potassium channels in secretory cells.
abstract: In exocrine acinar cells (pancreas, salivary gland, lacrimal gland) stimulation with hormones or neurotransmitters evokes K+ loss due to opening of K+ channels in the plasma membrane whereas in the insulin-secreting pancreatic beta-cells, stimulation with glucose or glyceraldehyde evokes membrane depolarization due to closure of K+ channels. By measuring directly the small K+ currents flowing through single channels, in electrically isolated patches of plasma membrane of intact cells, it can be shown that stimulants having no direct access to the small membrane area from which recording is made can influence the pattern of channel opening. In the case of hormonal activation of exocrine acinar cells, Ca2+ is the final messenger and the K+-selective channel involved in the response has a high unit conductance, is very voltage sensitive and can be blocked by external tetraethylammonium. In the case of the insulin-secreting cells, the K+ channel which is inhibited by metabolic stimulation is a voltage-insensitive, inward rectifier which can be blocked by quinine. In experiments on permeabilized cells or cell-free excised, inside-out, membrane patches it can be shown that ATP evokes channel closure and ATP produced by glycolysis may therefore function as the internal messenger.
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology; D005088:Exocrine Glands / Q000502:physiology*; D006728:Hormones / Q000502:physiology; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D007515:Islets of Langerhans / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D008954:Models, Biological; D018377:Neurotransmitter Agents / Q000502:physiology; D010179:Pancreas / Q000502:physiology; D011188:Potassium / Q000378:metabolism*; D011803:Quinine / Q000494:pharmacology
chemical_list: D006728:Hormones; D007473:Ion Channels; D018377:Neurotransmitter Agents; D011803:Quinine; D011188:Potassium; D002118:Calcium