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.