An alpha‐adrenergic receptor mechanism controlling potassium permeability in the rat lacrimal gland acinar cell.

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Abstract
Rat lacrimal gland slices, incubated in a balanced, buffered salt solution, were physiologically stable for up to 2 h with respect to O2 consumption, extracellular space, and water and ion content. The release of 86Rb serves as a good substitute for 42K in monitoring the movement of K through the cell membrane. Adrenaline (epinephrine) appears to increase membrane permeability to K as evidenced by an increase in the rate of 86Rb efflux. This response to adrenaline was blocked by phentolamine but not by propranolol and was mimicked by phenylephrine but not by isoprenaline. The magnitude of the 86Rb release indicates that it is being released, at least in part from the lacrimal gland acinar cell. The lacrimal gland acinar cell has an .alpha.-adrenergic receptor, activation of which leads to an increase in membrane permeability to K.