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Vascular capacitance vessels refer to blood vessels—primarily veins and venules—that can distribute and store large volumes of blood with minimal changes in pressure, acting as a blood reservoir[1][3][6]. About 60–70% of total blood volume is sequestered in these vessels at rest[1][6]. They are highly compliant (distensible) and play a critical role in regulating cardiac preload, venous return, and arterial blood pressure by controlling how much blood is shifted between the peripheral venous system (capacitance vessels) and the central circulation[1][3][5]. Pharmacologic intervention on capacitance vessels is a foundational strategy in the management of conditions such as heart failure and hypertension, but the vessels themselves are not single molecular targets, receptors, or enzymes—they represent an anatomical and functional classification of the venous system[1][3][6][5][9]. Note: "Vascular capacitance vessels" is a physiological concept and vessel classification, not a molecule or drug target. Thus, it is not appropriate to treat it as a canonical molecular target; this term is most useful in cardiovascular physiology and clinical medicine when considering the hemodynamic properties of veins and related blood reservoirs[6][1][3][5].
- Venodilation (increasing capacitance, lowering preload and venous return; e.g., nitrates) - Venoconstriction (decreasing capacitance, increasing venous return; e.g., alpha-adrenergic agonists)
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