Potassium channel dysfunction plays a role in the pathogenesis of a number of vascular diseases including pulmonary and systemic hypertension, diabetes, and complications of atherosclerosis. Two types of K+ channels that are known to be prevalent and contribute significantly to the repolarization of vascular smooth muscle cell (SMC) membranes are the high-conductance Ca2+- and voltage-activated K+ (BKCa) channels, and the voltage-gated K+ (KV) channels. Alterations in either BKCa or KV channel function can have dramatic effects on vascular tone. To date, hereditary and congenital mutations in genes encoding K+ channels, abnormalities in transcription, posttranslational modifications, and altered responses to intracellular second messengers have been described as potential mechanisms for several cardiovascular diseases. Comprehensive approaches including genetic, biochemical, molecular biological, and electrophysiological analyses are necessary to identify the levels at which K+ channel expression patterns or function are disrupted. Additionally, reproducing clinical pathologies in animal, organ, and virtual models has been important in studying the discrete mechanisms by which the structure and function of these channels are altered in pathophysiological conditions. This article will describe approaches that are currently used to identify abnormalities in BKCa and KV channels that may exist in diseases involving vascular dysfunction.
- Potassium channel
- Smooth muscle