2. The nongenomic action, which has a rapid onset (minutes), is reversible (short duration of 60-90 minutes), and is dose dependent. A protective effect was demonstrated 2 hours after a single dose of 100 mcg of fluticasone propionate inhaler using bronchial provocation with cyclic adenosine monophosphate (cAMP). Higher doses were reported to cause more significant effects. Asthmatics present a significant increase in airway mucosal blood flow in comparison with healthy subjects. Calculated as in the volume of the conducting airways from the trachea to the terminal bronchioles, mean airway blood flow values were 24-77% higher in asthmatics than in healthy controls. The inhalation of fluticasone (880 mcg) or budesonide (400 mcg) significantly decreases blood flow in both groups, but more in asthmatics. Evidence suggests that CS decrease airway blood flow by modulating sympathetic control of vascular tone. CS inhibit the extra-neuronal monoamine transporter- mediated uptake of norepinephrine by bronchial arterial smooth muscle cells, therefore, potentiating noradrenergic neurotransmission in the airway vasculature. This action is possibly mediated by binding of CS to membrane bound GR in smooth muscle cells of human airway blood vessels. This effect is a topical local one and is a feature of Inhaled CS (ICS) rather that systemic CS (SCS). Furthermore, this decrease in airway blood flow is likely to enhance the action of inhaled bronchodilators by diminishing their clearance from the airway. Thus, simultaneous administration of ICS and bronchodilators could be of clinical significance. Accordingly, ICS would have to be administered simultaneously with bronchodilators in high and repeated or sequential doses as a way to obtain and maintain the effect throughout the time. Since ICS induced vasoconstriction peaks between 30 and 60 min after drug administration, their use in intervals not more that 30 min seems adequate.