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Inhaled corticosteroids: effects on the airway vasculature in bronchial asthma

¹ Division of Pulmonary and Critical Care Medicine, University of Miami School of Medicine, Miami, FL, USA, and ² Dept of Respiratory Medicine, Semmelweis University Budapest, School of Medicine, Hungary.

CORRESPONDENCE: A. Wanner, Division of Pulmonary and Critical Care Medicine, University of Miami School of Medicine, P.O. Box 016960 (R-47), Miami, FL 33101, USA. Fax: 1 3052436992. E-mail: AWanner{at}med.miami.edu

Keywords: Airway vascularity, angiogenesis, asthma, inhaled corticosteroids, nongenomic action, vasoconstriction

Received: April 21, 2005
Accepted July 22, 2005

Inhaled corticosteroids suppress airway inflammation and components of airway remodelling in bronchial asthma. In the tracheobronchial (airway) vasculature, these include the inhibition of inflammatory hyperperfusion, microvascular hyperpermeability, mucosal oedema formation, and the formation of new blood vessels (angiogenesis).

Corticosteroids are now known to exert their effects on the airway vasculature through genomic and nongenomic mechanisms. Genomic actions involve the regulation of target genes, and suppress most of the vascular elements of inflammation and angiogenesis in the airway. In contrast, nongenomic actions are mediated by rapid cellular mechanisms, and induce transient vasoconstriction in the airway, thereby reversing inflammatory hyperperfusion.

The vascular actions of corticosteroids contribute to controlling clinical symptoms of asthma primarily by influencing airway calibre in the lung periphery and airway hyperreactivity.

In this review article, recent advances into the understanding of cellular mechanisms and the clinical implications of the interaction of inhaled corticosteroids and the airway vasculature in asthma are reviewed.

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