title: Activation by calcium of membrane channels for potassium in exocrine gland cells.
abstract: In the rat parotid salivary gland, fluid secretion is regulated by alterations in fluxes of monovalent ions. In vitro, stimulation of muscarinic, alpha-adrenergic or substance P receptors provokes a biphasic increase in membrane permeability to K+ which can be conveniently assayed as efflux of 86Rb. The increased 86Rb flux is thought to arise in response to a receptor mediated elevation in [Ca2+]i which activates Ca2+-activated K+-channels. The biphasic nature of the response is presumably due to a biphasic mode of Ca2+ mobilization by secretagogues; a transient response reflects release of a finite pool of Ca from an intracellular store while a more sustained phase results from Ca entry through receptor operated Ca channels or gates. Calcium also mediates an increased Na+ entry which in turn activates the Na+, K+-pump. The mechanism involved in the regulation of monovalent ion channels by Ca2+ is not understood.
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D006152:Cyclic GMP / Q000378:metabolism; D004537:Eicosanoic Acids / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism*; D008954:Models, Biological; D010306:Parotid Gland / Q000378:metabolism*; D018129:Phosphatidylinositol Phosphates; D010716:Phosphatidylinositols / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
chemical_list: D004537:Eicosanoic Acids; D007473:Ion Channels; D018129:Phosphatidylinositol Phosphates; D010716:Phosphatidylinositols; D002217:Carbachol; D012964:Sodium; D006152:Cyclic GMP; D012413:Rubidium; D011188:Potassium; D002118:Calcium