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Vascular smooth muscle potassium channels are a heterogeneous group of ion channels that play a central role in the regulation of vascular tone and blood pressure. This group includes large-conductance calcium-activated (BKCa), ATP-sensitive (KATP), voltage-gated (Kv), and inward-rectifier (Kir) potassium channels [1, 2]. By facilitating the efflux of potassium ions, these channels maintain the resting membrane potential of vascular smooth muscle cells; their activation leads to hyperpolarization, which inhibits the entry of calcium through voltage-gated channels and results in vasodilation [2, 3]. Conversely, the closure or inhibition of these channels leads to depolarization and vasoconstriction. These channels are significant therapeutic targets for cardiovascular diseases, with drugs like minoxidil and diazoxide acting as KATP channel openers to treat severe hypertension [4, 5]. However, their clinical use is often complicated by systemic side effects such as reflex tachycardia and fluid retention [5].
Activation of these channels increases potassium efflux, leading to membrane hyperpolarization, closure of voltage-gated calcium channels, and subsequent smooth muscle relaxation.
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