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This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/C860    most recent 00526.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Walcott, B. Articles by Brink, P. R. Search for Related Content PubMed PubMed Citation Articles by Walcott, B. Articles by Brink, P. R.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Fluid secretion and the Na⁺-K⁺-2Cl^– cotransporter in mouse exorbital lacrimal gland

¹Centre for Visual Sciences, Research School of Biological Sciences, Australian National University, Canberra, Australia; and ²Department of Physiology and Biophysics, Health Sciences Center, State University of New York, Stony Brook, New York

Submitted 28 October 2004 ; accepted in final form 21 May 2005

We have previously suggested that fluid flow in the mouse exorbital lacrimal gland is driven by the opening of apical Cl^– and K⁺ channels. These ions move into the lumen of the gland and water follows by osmosis. In many tissues, the Na⁺-K⁺-2Cl^– cotransporter (NKCC1) replaces the Cl^– and K⁺ ions that move into the lumen. We hypothesize that mouse exorbital lacrimal glands would have NKCC1 cotransporters and that they would be important in fluid transport by this gland. We used immunocytochemistry to localize NKCC1-like immunoreactivity to the membranes of the acinar cells as well as to the basolateral membranes of the duct cells. We developed a method to measure tear flow and its composition from mouse glands in situ. Stimulation with the acetylcholine agonist carbachol produced a peak flow followed by a plateau. Ion concentration measurements of this stimulated fluid showed it was high in K⁺ and Cl^–. Treatment of the gland with furosemide, a blocker of the NKCC1 cotransporter, reduced the plateau phase of fluid flow by 30%. Isolated cells exposed to a hypertonic shock shrank by 20% and then showed a regulatory volume increase (RVI). Both the RVI and swelling were blocked by treatment with furosemide. Cells isolated from these glands shrink by 10% in the presence of carbachol. Blocking NKCC1 with furosemide reduced the amount of shrinkage by 50%. These data suggest that NKCC1 plays an important role in fluid secretion by the exorbital gland of mice.

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