Department of Cell Physiology and Molecular Biophysics, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.
Pulm Pharmacol Ther. 2009 Oct;22(5):388-97. doi: 10.1016/j.pupt.2008.09.006. Epub 2008 Oct 19.
Airway hyper-responsiveness associated with asthma is mediated by airway smooth muscle cells (SMCs) and has a complicated etiology involving increases in cell contraction and proliferation and the secretion of inflammatory mediators. Although these pathological changes are diverse, a common feature associated with their regulation is a change in intracellular Ca(2+) concentration (Ca(2+)). Because the Ca(2+) itself is a function of the activity and expression of a variety of ion channels, in both the plasma membrane and sarcoplasmic reticulum of the SMC, the modification of this ion channel activity may predispose airway SMCs to hyper-responsiveness. Our objective is to review how ion channels determine the Ca(2+) and influence the function of airway SMCs and emphasize the potential of ion channels as sites for therapeutic approaches to asthma.
