vasodilatation

Vasodilatation, also known as vasodilation, is the widening of blood vessels due to relaxation of smooth muscle in the vessel walls, most often in arteries and arterioles. This increases regional blood flow and reduces vascular resistance, playing a central role in tissue perfusion, temperature regulation, and hemodynamic stability. It can be local, in response to tissue needs, or systemic under certain conditions.

Several mechanisms underlie vasodilatation. Endothelium-derived relaxing factors, especially nitric oxide (NO) and prostacyclin (PGI2), promote smooth muscle relaxation. NO is produced by endothelial nitric oxide synthase (eNOS) in response to stimuli such as shear stress and certain mediators, and it activates guanylate cyclase in smooth muscle to raise cGMP, causing relaxation. Prostacyclin raises cAMP to achieve a similar effect. Other factors include endothelium-derived hyperpolarizing factor (EDHF) and metabolic signals like increased CO2, decreased O2, low pH, adenosine, and lactate, which signal higher tissue demand. Temperature elevation and inflammatory mediators such as histamine and bradykinin can also induce vasodilatation.

Clinical relevance varies with context. Endothelial dysfunction impairs NO-mediated vasodilatation and is linked to hypertension, atherosclerosis, and diabetes. Excessive vasodilatation occurs in septic shock and anaphylaxis, contributing to hypotension. Pharmacologic vasodilators—nitrates, calcium channel blockers, ACE inhibitors, angiotensin II receptor blockers, hydralazine, minoxidil, and PDE5 inhibitors—are used to treat conditions such as hypertension, angina, and pulmonary hypertension by enhancing vasodilatation through different mechanisms. Measuring vasodilatation can involve perfusion imaging or flow-based techniques in research and clinical settings.