Vasoconstrictive

Vasoconstrictive describes anything that causes vasoconstriction, the narrowing of blood vessels. This results in reduced vessel diameter, increased vascular resistance, and often higher arterial blood pressure. Vasoconstriction plays a key role in regulating blood flow distribution and maintaining blood pressure during stress or blood loss.

The mechanism mainly involves contraction of vascular smooth muscle, typically mediated by alpha-1 adrenergic receptors on arterioles. Activation triggers Gq signaling, increasing intracellular calcium, activating myosin light-chain kinase, and promoting smooth muscle contraction. Other pathways and receptors, such as endothelin receptors, angiotensin II receptors, and vasopressin receptors, can also promote vasoconstriction in particular vascular beds.

Endogenous vasoconstrictors include norepinephrine and, in certain contexts, epinephrine; angiotensin II; endothelin-1; and vasopressin. Additional contributors are thromboxane A2 and cold-induced sympathetic activity, which collectively help regulate blood pressure and heat conservation.

Pharmacology and clinical use: vasoconstrictive agents are used to raise blood pressure in shock states (for example, norepinephrine and phenylephrine) and to prolong the effect of local anesthetics when combined with vasoconstrictors. They are also used as nasal decongestants (such as phenylephrine) for temporary relief. Risks include hypertension, reduced peripheral perfusion, ischemia, and tissue injury if extravasation occurs; caution is warranted in patients with vascular disease or Raynaud phenomenon.

See also: vasodilation.