Abstract

As suggested by Thaysen et al. (1954) and shown by Young and Schogel (1966) the primary saliva produced by the secretory endpieces (acini) of mammalian salivary glands is “plasmalike” and has a high concentration of chloride. Since the transepithelial potential difference is lumen negative in the secreting state (Lundberg 1957), the transport of Cl- across the secretory epithelium evidently occurs against an electrochemical gradient and has to be active. It is interesting that a model based on transcellular, active transport of Cl- was proposed by Lundberg as early as 1957. Subsequently, Lundberg’s “chloride pump” model was criticized (Yoshimura and Imai 1967; Petersen and Poulsen 1968, 1969; Petersen 1970, 1972) and the concept of a Cl- pump, i.e., transport of Cl- directly linked to cell metabolism, was abandoned. In many subsequent studies, attention was paid mainly to the role of cations in the secretion of primary saliva. However, Poulsen and Kristensen (1982) demonstrated that addition of a cholinergic agonist to a preparation of collagenase-isolated rat parotid acini preequili-brated with 36Cl- caused a reduction in the cellular content of the isotope by approximately 50% within 7 s, thus indicating an impressive stimulation-induced net efflux of Cl-.

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