Cellular mechanisms of drug interaction in bronchial asthma therapy: a role of genomic and extragenomic signaling systems
Abstract
The present review discusses data on cellular mechanisms of interaction of beta-adrenergic agonists and glucocorticoids which are a basis of beneficial asthma therapy being inhaled in common. We show that besides inhibition of myosin light chains beta-agonists can influence the smooth muscle cells modulating the Ca2+-channels’ activity due to cytoskeleton's proteins, and regulate the smooth muscle cell contraction independently on proteinkinase A. Moreover, the beta-agonists are able to stimulate gene expression and to control the initiation of programme cell death (apoptosis) like steroid hormones do. In turn the steroids can beinvolved to the pathogenesis of bronchial asthma without the expression of genes controlling inflammatory reactions, while the beta-agonists effect the inflammation via production of extracellular cyclic AMP and adenosine.
About the Authors
S. N. Orlov
Научно-исследовательский центр университета г. Монреаль;
Лаборатория физико-химии биомембран биологического факультета МГУ им. М.В.Ломоносова
Canada
Canada
G. G. Ryazhsky
Институт пульмонологии Минздрава РФ
Russian Federation
Russian Federation
A. S. Sokolov
Институт пульмонологии Минздрава РФ
Russian Federation
Russian Federation
A. G. Chuchalin
Институт пульмонологии Минздрава РФ
Russian Federation
Russian Federation
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Review
For citations:
Orlov S.N., Ryazhsky G.G., Sokolov A.S., Chuchalin A.G. Cellular mechanisms of drug interaction in bronchial asthma therapy: a role of genomic and extragenomic signaling systems. PULMONOLOGIYA. 2003;(1):56-62. (In Russ.)
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