Activation by calcium of membrane channels for potassium in exocrine gland cells.

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.