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

1. In the presence of extracellular Ca, adrenaline stimulated a large increase in the rate of K (86Rb) release from rat lacrimal slices, followed by a lower, more sustained rate. 2. In the absence of extracellular Ca, adrenaline elicited only a transient release of 86Rb. 3. The artificial introduction of Ca into the cytosol by the ionophore A‐23187 could also initiate the release of 86Rb. 4. 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. 5. 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. 6. It is concluded that the agonist‐induced release of K from the lacrimal gland consists of both 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. 7. It is also concluded that both alpha‐adrenergic and muscarinic receptor occupation activate a common, post‐receptor mechanism which may be responsible for both phases of K release.