Effects of β-adrenergic receptor activation on alveolar macrophage cytoplasmic motility

T. Fukushima, K. Sekizawa, Y. Jin, M. Yamaya, H. Sasaki, T. Takishima

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)


We studied the effects of fenoterol, a β-adrenoceptor agonist, on the cytoplasmic motility of alveolar macrophages (AM) from dog lungs in vitro. Four days after the instillation of Fe3O4 particles (3 mg/kg) into the lower lobe bronchus, AM were harvested by bronchoalveolar lavage. Remanent field strength (RFS) from the AM containing Fe3O4 particles (5 x 106 cells) was measured immediately after magnetization. RFS decreased with time due to particle rotation (relaxation), which is related to cytoplasmic motility of AM. Fenoterol (10-9 M to 10-5 M) decreased the relaxation rate (λ0; min-1) in a concentration-dependent fashion with the maximum effect at 10-6 M. Both forskolin (10-6 M to 10-4 M) and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) (10-3 M) mimicked fenoterol- induced inhibitory effects on λ0. Fenoterol and forskolin concentration- dependently increased intracellular levels of cAMP, which were parallel to decreases in λ0 induced by these drugs. KT 5720 (10-5 M), a specific inhibitor of protein kinase A, significantly inhibited fenoterol (10-6 M)- induced inhibitory effects on λ0 (P < 0.01). These results imply that β- adrenergic receptor activation inhibits cytoplasmic motility of AM via increases in intracellular levels of cAMP, which may be coupled with activation of a cAMP-dependent protein kinase.

Original languageEnglish
Pages (from-to)L67-L72
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 9-1
Publication statusPublished - 1993


  • adenosine 3',5'-cyclic monophosphate
  • cholera toxin-sensitive G proteins
  • protein kinase A
  • remanent field strength

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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