TY - JOUR
T1 - Effects of salmeterol on secretion of phosphatidylcholine by alveolar type II cells
AU - Kumar, Vasanth H.S.
AU - Christian, Constance
AU - Kresch, Mitchell J.
N1 - Funding Information:
The authorsw ould like to acknowledget he help from Glaxo Wellcome Research& Development Limited. Uxbridge, Middlesex, UK for providing us with salmeterol. We would also like to acknowledge the suggestions from Dr. Malcolm Johnson of Glaxo Wellcome Research & DevelopmentL imited. UK and for reviewing the manuscript. This work was supportedin partb y a grant from Glaxo Wellcome Researcha nd DevelopmentL imited. Uxbridge. Middlesex. UK.
PY - 2000/3/17
Y1 - 2000/3/17
N2 - β-adrenergic agents enhance secretion of phosphatidylcholine (PC) by adult and fetal type II cells. We have previously shown that terbutaline stimulates 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 β-adrenergic agonist that does not cause receptor desensitization, on PC secretion by adult type II alveolar cells in primary culture. Release of lactate-dehydrogenase was < 4% and did not vary with the concentration of salmeterol. Salmeterol stimulated PC secretion in a concentration-dependent manner. The maximum effective-concentration tested was 50 nM and the EC50 was 11.40 ± 1.14 nM. Propranolol inhibited the effect of salmeterol on release of PC, confirming that the effects of salmeterol are mediated by β-receptors. OT50, the time for onset of action, was 32.0 ± 1.6 minutes. RT50, the time to achieve 50% recovery from maximal stimulation was, 393.0 ± 20.2 minutes. We conclude that salmeterol stimulates PC secretion by type II cells through activation of β- adrenergic receptors and has a longer duration of action (>6 hours) compared to other β2-agonists. Salmeterol may be a useful drug with which to study the role of receptor desensitization in the developmental changes in PC secretion.
AB - β-adrenergic agents enhance secretion of phosphatidylcholine (PC) by adult and fetal type II cells. We have previously shown that terbutaline stimulates 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 β-adrenergic agonist that does not cause receptor desensitization, on PC secretion by adult type II alveolar cells in primary culture. Release of lactate-dehydrogenase was < 4% and did not vary with the concentration of salmeterol. Salmeterol stimulated PC secretion in a concentration-dependent manner. The maximum effective-concentration tested was 50 nM and the EC50 was 11.40 ± 1.14 nM. Propranolol inhibited the effect of salmeterol on release of PC, confirming that the effects of salmeterol are mediated by β-receptors. OT50, the time for onset of action, was 32.0 ± 1.6 minutes. RT50, the time to achieve 50% recovery from maximal stimulation was, 393.0 ± 20.2 minutes. We conclude that salmeterol stimulates PC secretion by type II cells through activation of β- adrenergic receptors and has a longer duration of action (>6 hours) compared to other β2-agonists. Salmeterol may be a useful drug with which to study the role of receptor desensitization in the developmental changes in PC secretion.
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U2 - 10.1016/S0024-3205(00)00483-5
DO - 10.1016/S0024-3205(00)00483-5
M3 - Article
C2 - 11261593
AN - SCOPUS:0034677971
SN - 0024-3205
VL - 66
SP - 1639
EP - 1646
JO - Life Sciences
JF - Life Sciences
IS - 17
ER -