Further evidence for the functional relevance of β-AR in eosinophils is provided by results obtained in a model of airway inflammation induced in anesthetized rats by injecting substance P or bradykinin intravenously, where activation of β2-AR by the β2-AR agonist formoterol was shown to reduce the amount of plasma leakage and also the number of neutrophils and eosinophils that adhered to the vascular endothelium at sites of inflammation, an effect which could be antagonized by the β2-AR antagonist propranolol (Bowden Sulakvelidze and McDonald, 1994). The gene discussed is ADRB2; the disease is inflammation.