Inhaled β-agonists are effective at reversing bronchoconstriction in asthma, but the
mechanism by which they exert this effect is unclear and controversial. PKA is the historically
accepted effector, although this assumption is made on the basis of associative and not
direct evidence. Recent studies have asserted that exchange protein activated by cAMP
(Epac), not PKA, mediates the relaxation of airway smooth muscle (ASM) observed with β-
agonist treatment. This study aims to clarify the role of PKA in the prorelaxant effects of β …