Alveolar sodium and liquid transport in mice

We have developed a simple isolated lung preparation for measurement of liq uid and solute fluxes across mouse alveolar epithelium. Liquid instilled in to air spaces was absorbed at the rate (J(w)) of 3.7 +/- 0.32 ml.h(-1).g dr y lung wt(-1). 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 Naf-glucose cotransport inhibitor phloridzin did not affect J(w). Ho wever, the low epithelial lining fluid glucose concentration (one-third tha t of plasma), the larger-than-mannitol permeability of methyl-alpha-D-gluco pyranoside, and the presence of Na+-glucose cotransporter SGLT1 mRNA in mou se lung tissue suggest that there is a Na+-glucose cotransporter in the mou se alveolar-airway barrier. Isoproterenol stimulated J(w) (6.5 +/- 0.45 ml. h(-1).g dry lung wt(-1); P < 0.001), and this effect was blocked by amilori de, benzamil, ouabain, and the specific beta(2)-adrenergic antagonist ICI-1 18551 but not by atenolol. Similar stimulation was obtained with terbutalin e (6.4 +/- 0.46 ml.h(-1).g dry lung wt(-1)). Na+ unidirectional fluxes out of air spaces varied in agreement with J(w) changes. Thus alveolar liquid a bsorption 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.