Secretion of water and electrolytes in salivary glands occurs by a dual process involving the formation of a plasma-like, isotonic primary-secretion in salivary acini and its subsequent modification in salivary-ducts by the removal and addition of specific ions. The mechanisms underlying the formation of primary acinar secretion have been investigated with a number of experimental approaches such as electrophysiology, the measurement of ion transport in gland fragments and dispersed acinar cells, and the evaluation of the ionic requirements for secretion in isolated, perfused gland preparations. The accumulated evidence suggests that salivary secretion is formed by a complex interaction between passive and active ion movements across acinar cell membranes, resulting in the trans-acinar movement of CI and Na+ and, by the osmotic gradient which develops, of water. A major consequence of stimulation is the release of K + through Ca++ -and voltage-sensitive channels and its subsequent recycling back into the cells by ouabain- and furosemide-sensitive transport systems. This results in NaCl uptake across the basolateral cell membrane and the subsequent efflux of CI through luminal membrane channels, which also appear to be sensitive to cellular Ca + +. The rates of these various ion movements appear to be, therefore, closely linked and interdependent. Ductal modification of the primary secretion has been studied in microperfused duct preparations. The evidence likewise indicates that it involves interactions between complex conductance pathways in the luminal cell membrane and a Na, K pump present in the basolateral cell membrane and that it is under autonomic and hormonal control. Activation of ductal transport mechanisms results in NaCl reabsorption and KHCO3 secretion. Final saliva thus differs from primary secretion in electrolyte composition and, because water permeability is low in the duct epithelium, becomes hypotonic. Alterations in fluid and electrolyte secretion such as those observed in disease can result, therefore, from disturbances in one or more of these complex transport processes in acinar or duct cells.
Hormonally regulated phosphoprotein of turkey erythrocytes: localization to plasma membrane.
