The role of calcium in the receptor mediated control of potassium permeability in the rat lacrimal gland.

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Abstract
In the presence of extracellular Ca, adrenaline [epinephrine] stimulated a large increase in the rate of K (86Rb) release from rat lacrimal slices followed by a lower, more sustained rate. In the absence of extracellular Ca, adrenaline elicited only a transient release of 86Rb. The artificial introduction of Ca into the cytosol by the ionophore A-23187 could initiate the release of 86Rb. In a zero-Ca medium, if either adrenaline or carbachol produced a transient release of 86Rb, the tissue could not respond to the other agonist with a transient release unless Ca was momentarily reintroduced to the medium. If Ca was present in a limiting concentration, the Ca-dependent rate of 86Rb release elicited from a lacrimal slice exposed simultaneously to carbachol and adrenaline was not significantly different from the release seen with carbachol alone. The agonist-induced release of K from the lacrimal gland consists of a Ca-independent phase which is initiated by the release of a limited pool of Ca and a Ca-dependent phase which is mediated by the influx of extracellular Ca. Both .alpha.-adrenergic and muscarinic receptor occupation activated a common, post-receptor mechanism which may be responsible for both phases of K release.