Vasodilation

Vasodilation is the widening of blood vessels due to relaxation of the smooth muscle in their walls. This increases the diameter of the vessel lumen, reduces vascular resistance, and enhances blood flow to the affected tissues. Vasodilation can occur in arteries, arterioles, and veins, and venous dilation can decrease venous return and preload.

Mechanisms of vasodilation are broadly categorized as endothelium-dependent and endothelium-independent. Endothelium-dependent dilation is mediated by substances released from the vascular endothelium, most notably nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor (EDHF). NO is produced by nitric oxide synthase and activates soluble guanylate cyclase in smooth muscle, increasing cGMP and causing relaxation. Prostacyclin increases cAMP in smooth muscle, also promoting relaxation. EDHF causes hyperpolarization of the smooth muscle cell membrane, reducing calcium influx. Endothelium-independent mechanisms include direct effects on smooth muscle, such as activation of potassium channels or changes in cyclic nucleotide signaling via pharmacologic agents.

Physiologic regulation involves local factors linked to tissue needs, such as increased CO2, lactic acid, adenosine, temperature, and shear stress, which promote dilation to improve perfusion. Autonomic control generally favors vasoconstriction through sympathetic activity, though local and hormonal signals can override this in specific beds. Hormones and drugs can induce systemic vasodilation (eg, NO donors, nitrates, calcium channel blockers, or ACE inhibitors) or selective bed-specific dilation.

Clinical relevance includes regulation of blood pressure and tissue perfusion, heat dissipation, and responses to exercise. Abnormal vasodilation occurs in conditions such as sepsis and anaphylaxis, where widespread dilation can lead to hypotension. Pharmacologic vasodilators are used to treat hypertension, angina, heart failure, and erectile dysfunction.