Abstract
Potassium channels play a pivotal role in the regulation of excitability in cells such as neurons, cardiac myocytes, and vascular smooth muscle cells. The KCNQ (Kv7) family of voltage-activated K+ channels hyperpolarizes the cell and stabilizes the membrane potential. Here, we outline how Kv7 channel activity may contribute to the development of the cardiovascular risk factors such as hypertension, diabetes, and obesity. Questions and hypotheses regarding previous and future research have been raised. Alterations in the Kv7 channel may contribute to the development of cardiovascular disease (CVD). Pharmacological modification of Kv7 channels may represent a possible treatment for CVD in the future.
Highlights
In this review, we focus on the family of the Kv7 channel encoded by the KCNQ genes and explore their possible role in cardiovascular disease (CVD) and the risk factors hypertension (HT), obesity and diabetes.With more than 78 members, the voltage-dependent potassium channels (Kv) are the largest contributor to the superfamily of voltage-dependent ion channels in humans
HG was found to contribute to the rise in NADPH oxidase activity in coronary arteries. This effect was prevented by GW0742. These results suggest that the HG-induced Kv7 channel downregulation is a result of oxidative modulation
Similar studies have not been done on human tissue so far, these findings indicated that opening of Kv7 channels might improve impaired PVATmediated vasodilatation in obese-related HT
Summary
We focus on the family of the Kv7 channel encoded by the KCNQ genes and explore their possible role in cardiovascular disease (CVD) and the risk factors hypertension (HT), obesity and diabetes. Homotetramers of Kv7.1 in cardiomyocytes associate with the ancillary protein KCNE1 Together, they constitute the functional channels that give rise to the slowly activating IKS current [13], which plays a central role in ventricular repolarization [5, 6, 15]. It has been shown that hyperglycemia (HG) in diabetic rats resulted in reduced Kv7 channel activity, expression, and vasodilatory function in the left coronary artery [32]. A study involving 14 patients diagnosed with KCNQ1 long QT syndrome showed increased postprandial insulin release in KCNQ1 mutation carriers compared with two control participants They displayed higher β-cell glucose sensitivity and lower levels of plasma glucose and serum potassium upon oral glucose stimulation. If autoantibodies against the NH2-terminal of the β-subunit would exist, the result could be non-functional Kv7 channels and development of CV risk factors such as HT, diabetes and obesity
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