October 1991
Volume 32, Issue 11
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Articles  |   October 1991
Secretagogue-induced redistributions of Na,K-ATPase in rat lacrimal acini.
Author Affiliations
  • S C Yiu
    Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033.
  • R W Lambert
    Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033.
  • P J Tortoriello
    Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033.
  • A K Mircheff
    Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033.
Investigative Ophthalmology & Visual Science October 1991, Vol.32, 2976-2984. doi:
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      S C Yiu, R W Lambert, P J Tortoriello, A K Mircheff; Secretagogue-induced redistributions of Na,K-ATPase in rat lacrimal acini.. Invest. Ophthalmol. Vis. Sci. 1991;32(11):2976-2984.

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Abstract

Lacrimal acinar cells secrete macromolecular products in an approximately isotonic, sodium chloride (NaCl)-rich fluid. The mechanisms of macromolecular product secretion depend in part on a recycling traffic of membrane constituents between the Golgi complex and the apical plasma membrane. In contrast, the acinar cell's mechanisms for secreting Na+ and Cl- depend largely on the fluxes of these ions through transporters expressed in the apical and basal-lateral membranes. In addition to accelerating the recycling of secretory vesicle membrane constituents, the cholinergic agonist carbachol also triggers a net redistribution of sodium potassium adenosine triphosphatase (Na,K-ATPase) ion pumps between Golgi-associated pools and the basal-lateral plasma membranes (Yiu SC, et al: J Membrane Biol 102:185, 1988). In the present study, acinar preparations from rat lacrimal glands were stimulated with either carbachol, epinephrine, or isoproterenol. All three agonist stimulated release of the secretory protein lactoperoxidase, but only carbachol significantly accelerated Na+ undirectional influx. Subcellular fractionation analyses of resting and stimulated preparations indicated that carbachol caused a significant translocation of Na,K-ATPase activity from a Golgi-associated compartment to the basal-lateral plasma membranes. Neither adrenergic agonist significantly increased the basal-lateral membrane Na,K-ATPase activity, but each triggered a distinct pattern of redistributions of Na,K-ATPase and the Golgi membrane marker, galactosyltransferase. The carbachol-induced augmentation of basal-lateral membrane Na,K-ATPase activity represents a mechanism by which the cell might compensate for increased Na+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)

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