Peripheral vascular resistance (PVR (also commonly referred to as SVR for systemic vascular resistance))

Peripheral vascular resistance is **not a molecule or receptor**, but rather a physiological parameter describing the **resistance to blood flow offered by the systemic arteries and arterioles**. It is a key determinant in the regulation of arterial blood pressure and tissue perfusion. The main factors influencing it are vessel diameter, blood viscosity, and vessel length. Increased peripheral vascular resistance is associated with conditions such as hypertension and heart failure; decreased PVR can occur in shock states. While drugs can target mechanisms that alter PVR—such as vasodilators or agents affecting smooth muscle tone—PVR itself is not a direct therapeutic target like an enzyme or receptor but rather an outcome influenced by multiple molecular targets[1][4][7]. "Peripheral vascular resistance... refers to the resistance to blood flowing through the arteries and arterioles in the peripheral circulation... plays a vital role in maintaining blood pressure..."[1] "Peripheral vascular resistance... is used to create blood pressure, [and] is also a component of cardiac function. When vessels constrict this leads to an increase in SVR..."[4] Because it describes a hemodynamic property—not a discrete protein, gene product, or molecular entity—it should not be classified as a canonical drug target for structured pharmacological databases.

Other names

Total peripheral resistanceSystemic vascular resistance (SVR)Vascular resistanceTPR (Total peripheral resistance)

Vasodilation to decrease peripheral vascular resistance and lower blood pressure[1][4] Vasoconstriction to increase peripheral vascular resistance when needed for physiological compensation[4][7]