Chloride fluxes during cAMP stimulation of liquid absorption across the native rat alveolar epithelium

cAMP activates Cl- channels in the alveolar epithelium of rabbits (Nielsen et al. Am J Physiol. 1998; 275:L1127-L1133), resulting in Cl- secretion; an d of rats (Jiang et al. Am J Physiol. 1998; 275:C1610-C1620), resulting in Cl- absorption. The relationship between Cl- fluxes and liquid absorption a cross the alveolar barrier was examined using isolated perfused rat lungs. Unidirectional Cl-36(-) fluxes (apparent PACl products) in the apical-to-ba sal (absorption, PACl(ab)) and reverse (secretion, PACl(ba)) directions wer e identical tinder control conditions. Both increased about 2-fold during s timulation of liquid absorption by dibutyrylcAMP + isobutylmethylxanthine ( P <.001). Inhibiting Na+ and liquid absorption during cAMP stimulation by a dding amiloride to the alveolar instillate decreased PA Cl-ab to control le vel (P <.01), but did not affect PA Cl-ba. Neither alveolar liquid absorpti on nor PACl(ba) was affected by apical N-phenylanthranilic acid or basolate ral bumetanide during cAMP stimulation. Mannitol permeability-surface area products did not differ with the experimental condition. These observations indicate that cAMP stimulation results in enhanced Cl- and liquid absorpti on from rat airspaces and Cl- secretion into them. They suggest that Cl- ab sorption follows Na+ transport, but fail to demonstrate any significant par ticipation of cAMP-activated Cl- channels in these changes.