β-Adrenergic agonists are used in the treatment of bronchial asthma for their bronchodilator effect, in addition, they may have anti-allergic effects. We investigated the effects of procaterol, a long acting β
2 agonist, on human inflammatory cells including monocytes, neutrophils, basophils and lung mast cells. Procaterol caused dose-related inhibition of thromboxane B
2 (TXB
2) release from monocytes (63.43±3.36% at 10
-5 M of procaterol: percentage of control TXB
2 release) ; this effect was completely abolished by propranolol, suggesting that it is mediated via β
2 receptors. In contrast, there was no inhibition of N-acetyl-β-D-glucosaminidase (NAG) release. Further, procaterol dosedependently inhibited superoxide anion release from neutrophils (40.99±10.74% at 10
-5 M: percentage of control O
2-·release), which was partially reduced by propranolol. Procaterol had no effect on f ormyl-Methionyl-Leucyl-Phenylala-nine (FMLP) -induced neutrophil chemotaxis.Procaterol dose-dependently inhibited lung mast cell histamine release after anti-IgE challenge (59.66±6.13% at 10
-5M) ; this effect was completely abolished by pre-treatment with propranolol. Procaterol (10
-4M) only inhibited basophil histamine release 5 min after anti-IgE stimulation. Thus, procaterol, has inhibitory effects on some but not all functions of human monocytes, neutrophils, basophils, and mast cells.
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