Cholera Toxin Stimulates Secretion of Saturated Phosphatidylcholine and Increases Cellular Cyclic AMP in Isolated Rat Alveolar Type II Cells

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Abstract
The time course was compared of saturated phosphatidylcholine secretion and cellular cyclic [c] AMP concentrations in isolated rat alveolar type-II cells following stimulation by cholera toxin, terbutaline and 12-O-tetradecanoyl-phorbol-1-13-acetate. Secretion of saturated phosphatidylcholine was stimulated by cholera toxin at concentrations from 1.2 .times. 10-11 M-5.0 .times. 10-7 M. In time course experiments there was no significant stimulation with cholera toxin before 1 h; all subsequent points between 90 and 180 min were significantly different from controls. Secretion stimulated by 10-.mu.M terbutaline was similar in magnitude to stimulation by 1.2 .times. 10-9 M cholera toxin; stimulation following either of these agonists was higher than control secretion and lower than secretion stimulated by 10-nM 12-O-tetradecanoyl-phorbol-13-acetate. Terbutaline caused an early rise in cellular-cAMP that peaked within 5 min and then returned to basal level by 60 min. Cholera toxin did not increase cellular cAMP levels until 60 min after addition, but then produced a sustained increase in cAMP levels for up to 3 h. More than one mechanism exists by which secretion can be stimulated in type-II cells. It is likely that both terbutaline and cholera toxin act by stimulating cellular cAMP and that 12-O-tetradecanoyl-phorbol-13-acetate acts by a mechanism different from terbutaline or cholera toxin.

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