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Am J Physiol. 1999 Dec;277(6):L1232-8. doi: 10.1152/ajplung.1999.277.6.L1232.

Alveolar sodium and liquid transport in mice.

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Service de Chirurgie Thoracique et Cardiovasculaire, Centre Hospitalier Universitaire de Caen, 14000 Caen, France.


We have developed a simple isolated lung preparation for measurement of liquid and solute fluxes across mouse alveolar epithelium. Liquid instilled into air spaces was absorbed at the rate (J(w)) of 3.7 +/- 0.32 ml x h(-1) x g dry lung wt(-1) x J(w) was significantly depressed by ouabain (P < 0.001) and amiloride (P < 0.001). Omission of glucose from the instillate or addition of the Na(+)-glucose cotransport inhibitor phloridzin did not affect J(w). However, the low epithelial lining fluid glucose concentration (one-third that of plasma), the larger-than-mannitol permeability of methyl-alpha-D-glucopyranoside, and the presence of Na(+)-glucose cotransporter SGLT1 mRNA in mouse lung tissue suggest that there is a Na(+)-glucose cotransporter in the mouse alveolar-airway barrier. Isoproterenol stimulated J(w) (6.5 +/- 0.45 ml x h(-1) x g dry lung wt(-1); P < 0.001), and this effect was blocked by amiloride, benzamil, ouabain, and the specific beta(2)-adrenergic antagonist ICI-118551 but not by atenolol. Similar stimulation was obtained with terbutaline (6.4 +/- 0.46 ml x h(-1) x g dry lung wt(-1)). Na(+) unidirectional fluxes out of air spaces varied in agreement with J(w) changes. Thus alveolar liquid absorption in mice follows Na(+) transport via the amiloride-sensitive pathway, with little contribution from Na(+)-glucose cotransport, and is stimulated by beta(2)-adrenergic agonists.

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