Vasoconstriction

Vasoconstriction is the narrowing of blood vessels caused by contraction of vascular smooth muscle, most commonly in arterioles. This constriction increases vascular resistance and can raise arterial blood pressure. It can occur as part of normal physiologic regulation or in response to stress, cold, or injury.

Molecularly, constriction involves increased intracellular calcium in smooth muscle cells, leading to activation of myosin light-chain kinase and phosphorylation of myosin light chains, enabling contraction. Receptor-mediated pathways include alpha-1 adrenergic receptors activated by norepinephrine and epinephrine, endothelin receptors, and angiotensin II type 1 receptors. The endothelium modulates tone by releasing vasodilators such as nitric oxide and prostacyclin; if endothelial dysfunction or dominant constrictors prevail, vasoconstriction is enhanced. Autonomic reflexes, particularly baroreceptor-mediated sympathetic discharge, can rapidly produce systemic vasoconstriction to preserve perfusion during hypotension or standing.

Physiologically, vasoconstriction redirects blood flow to essential organs and helps regulate blood pressure. Pathologically, excessive or inappropriate vasoconstriction can impair tissue perfusion, contributing to conditions such as frostbite, cold-induced Raynaud phenomenon, myocardial or cerebral ischemia during vasospasm, and shock.

Therapeutically, vasoconstriction is a target in clinical care: vasopressor drugs such as norepinephrine or phenylephrine are used to raise blood pressure in hypotensive states, whereas vasodilators are used to counteract unwanted vasoconstriction in conditions like Raynaud phenomenon or hypertensive emergencies. Endothelial balance between vasoconstrictors and vasodilators governs vascular tone under varying conditions.