Effects of salmeterol on secretion of phosphatidylcholine by alveolar typeII cells

beta-adrenergic agents enhance secretion of phosphatidylcholine (PC) by adu lt and fetal type II cells. We have previously shown that terbutaline stimu lates secretion of PC by fetal type II cells, but the response wanes after 30 minutes. We studied the effects of salmeterol, a highly selective, long- acting beta(2)-adrenergic agonist that does not cause receptor desensitizat ion, on PC secretion by adult type II alveolar cells in primary culture. Re lease of lactate-dehydrogenase was < 4% and did not vary with the concentra tion of salmeterol. Salmeterol stimulated PC secretion in a concentration-d ependent manner. The maximum effective-concentration tested was 50 nM and t he EC50 was 11.40 +/- 1.14 nM. Propranolol inhibited the effect of salmeter ol on release of PC, confirming that the effects of salmeterol are mediated by P-receptors. OT50, the time for onset of action, was 32.0 +/- 1.6 minut es. RT50, the time to achieve 50% recovery from maximal stimulation was, 39 3.0 +/- 20.2 minutes. We conclude that salmeterol stimulates PC secretion b y type II cells through activation of beta-adrenergic receptors and has a l onger duration of action (>6 hours) compared to other beta(2)-agonists. Sal meterol may be a useful drug with which to study the role of receptor desen sitization in the developmental changes in PC secretion.