Abstract
cAMP activates Cl- channels in the alveolar epithelium of rabbits (Nielsen et al. Am J Physiol. 1998; 275:L1127 L1133), resulting in Cl- secretion; and of rats (Jiang et al. Am J Physiol. 1998; 275:C1610 C1620), resulting in Cl- absorption. The relationship between Cl- fluxes and liquid absorption across the alveolar barrier was examined using isolated perfused rat lungs. Unidirectional 36 Cl- fluxes (apparent PACl products) in the apical-to-basal (absorption, PAClab) and reverse (secretion, PAClba) directions were identical under control conditions. Both increased about 2-fold during stimulation of liquid absorption by dibutyrylcAMP + isobutylmethylxanthine (P <. 001). Inhibiting Na+ and liquid absorption during cAMP stimulation by adding amiloride to the alveolar instillate decreased PAClab to control level (P <. 01), but did not affect PAClba. Neither alveolar liquid absorption nor PAClba was affected by apical N-phenylanthranilic acid or basolateral 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 absorption from rat airspaces and Cl- secretion into them. They suggest that Cl- absorption follows Na+ transport, but fail to demonstrate any significant participation of cAMP- activated Cl channels in these changes.