Abstract
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+)](i)). Because the [Ca(2+)](i) 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+)](i) and influence the function of airway SMCs and emphasize the potential of ion channels as sites for therapeutic approaches to asthma.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Asthma / metabolism
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Asthma / pathology
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Asthma / physiopathology*
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Bronchial Hyperreactivity / metabolism
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Bronchial Hyperreactivity / pathology
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Calcium / metabolism*
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Calcium Signaling / physiology*
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Humans
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Inflammation / metabolism
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Intracellular Fluid / metabolism
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Ion Channels / metabolism
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Ion Channels / physiology*
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Models, Biological
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Muscle Cells / metabolism
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Muscle Cells / pathology
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Muscle Cells / physiology*
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Muscle, Smooth / metabolism
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Muscle, Smooth / pathology
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Muscle, Smooth / physiology*
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Muscle, Smooth / physiopathology
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Potassium Channels, Calcium-Activated / metabolism
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Potassium Channels, Calcium-Activated / physiology
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Respiratory System / metabolism
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Respiratory System / pathology
Substances
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Ion Channels
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Potassium Channels, Calcium-Activated
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Calcium