Journal
EXPERT OPINION ON THERAPEUTIC TARGETS
Volume 14, Issue 8, Pages 825-837Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1517/14728222.2010.500616
Keywords
calcium-activated potassium channels; cardiovascular disease; endothelial cell calcium; endothelial nitric oxide synthase; L-arginine; NADPH oxidase; nitric oxide; reactive oxygen species; vascular endothelium
Categories
Funding
- Lundbeck Foundation
- Danish Cardiovascular Research Academy
- Danish Medical Research Council
- Faculty of Health Sciences, Aarhus University
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Importance of the field: Cardiovascular risk factors are often associated with endothelial dysfunction, which is also prognostic for occurrence of cardiovascular events. Endothelial dysfunction is reflected by blunted vasodilatation and reduced nitric oxide (NO) bioavailability. Endothelium-dependent vasodilatation is mediated by NO, prostacyclin, and an endothelium-derived hyperpolarising factor (EDHF), and involves small (SK) and intermediate (IK) conductance Ca2+-activated K+ channels. Therefore, SK and IK channels may be drug targets for the treatment of endothelial dysfunction in cardiovascular disease. Areas covered in this review: SK and IK channels are involved in EDHF-type vasodilatation, but recent studies suggest that these channels are also involved in the regulation of NO bioavailability. Here we review how SK and IK channels may regulate NO bioavailability. What the reader will gain: Opening of SK and IK channels is associated with EDHF-type vasodilatation, but, through increased endothelial cell Ca2+ influx, L-arginine uptake, and decreased ROS production, it may also lead to increased NO bioavailability and endothelium-dependent vasodilatation. Take home message: Opening of SK and IK channels can increase both EDHF and NO-mediated vasodilatation. Therefore, openers of SK and IK channels may have the potential of improving endothelial cell function in cardiovascular disease.
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