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Vascular smooth muscle (VSM) refers to the specialized smooth muscle tissue located within the walls of blood vessels, including the coronary and peripheral arteries. Its primary biological function is the regulation of vascular tone, which determines the diameter of the vessel lumen and thereby controls blood flow and systemic blood pressure [1]. In the coronary arteries, VSM relaxation is essential for increasing myocardial blood flow during periods of high oxygen demand, while in peripheral vessels, VSM contraction maintains total peripheral resistance [2]. Pathological dysfunction of VSM, including excessive contraction or phenotypic switching to a proliferative state, is a hallmark of cardiovascular diseases such as hypertension, atherosclerosis, and restenosis [3]. While VSM is a tissue rather than a single molecular target, it contains numerous proteins that serve as drug targets, such as L-type calcium channels, alpha-1 adrenergic receptors, and potassium channels [4]. Pharmacological intervention typically aims to induce vasodilation to treat conditions like angina pectoris and hypertension [5].
Drugs targeting vascular smooth muscle primarily act by modulating the concentration of intracellular calcium ions or the sensitivity of the contractile machinery to calcium. This is achieved through the inhibition of L-type voltage-gated calcium channels, the activation of soluble guanylate cyclase via nitric oxide release, or the antagonism of G protein-coupled receptors such as the alpha-1 adrenergic receptor.
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