vasoconstriktory

Vasoconstrictors are agents that cause vasoconstriction, the narrowing of blood vessels, which increases vascular resistance and arterial pressure. They influence regional blood flow and can modify capillary perfusion depending on tissue and dose. In physiology, several endogenous systems regulate vasoconstriction as part of the body’s response to stress or dehydration.

Endogenous vasoconstrictors include norepinephrine and epinephrine, angiotensin II, vasopressin (antidiuretic hormone), and endothelin-1. They act on vascular smooth muscle through receptors such as alpha-1 adrenergic receptors and specific vasopressin or endothelin receptors, triggering signaling cascades that raise intracellular calcium and promote contraction.

Pharmacologic vasoconstrictors, often called vasopressors, are used clinically to raise blood pressure or reduce bleeding. Common agents include norepinephrine, phenylephrine, epinephrine, vasopressin, and, at higher doses, dopamine. In addition, topical or intranasal vasoconstrictors such as phenylephrine or oxymetazoline are used to relieve nasal congestion or control local bleeding. Angiotensin II analogues have been developed for vasodilatory shock unresponsive to other therapies.

Adverse effects can include hypertension, tachycardia, reduced perfusion to organs, and tissue injury from extravasation of infusions. They require careful patient selection, dosing, and monitoring, particularly in individuals with cardiovascular disease, peripheral vascular disease, or renal impairment.

See also: vasopressor, vasodilation, blood pressure regulation.