Table 1.

Molecular and cellular effects of αAR-agonists and glucocorticoids in the upper airway.

Treatment modality	Physiological effects
αAR-agonists	(i) Increased vascular smooth muscle (VSM) contractile tone
	Gq protein-mediated VSM contraction (α1)
	Gi protein-mediated VSM impaired relaxation (α2)
	(ii) Modulation of mucosa blood flow and thickness
	(iii) Increased nasal cavity cross-sectional area
	(iv) Increased oropharyngeal patency
	(v) Increased subglottic intraluminal diameter
Glucocorticoids	(i) Transrepression of AP-1 and NF-κB transcription factors
	(ii) Regulation of mitogen-activated protein kinases (MAPKs)
	(iii) Modulation of vascular endothelial growth factor (VEGF) expression
	(iv) Enhanced αAR-signaling and prevention of αAR-homologous desensitization
	(v) Modulation of airway mucosa inflammation
	(vi) Reduced airway mucosa thickness
	(vii) Increased nasal and subglottic patency