Vasoconstrictors

Vasoconstrictors are substances that narrow blood vessels by contracting vascular smooth muscle, thereby increasing vascular resistance and arterial pressure. They include endogenous mediators such as norepinephrine, epinephrine, angiotensin II, vasopressin, and endothelin, as well as therapeutic drugs used to manipulate vascular tone. In clinical practice they can act systemically to support blood pressure or locally to reduce bleeding or congestion. Some agents are used topically or locally because they produce focal vasoconstriction with limited systemic effects.

Most vasoconstrictors act on vascular smooth muscle through specific receptors. Alpha-1 adrenergic receptors drive contraction via phospholipase C and increased intracellular calcium. Angiotensin II acts through AT1 receptors, vasopressin through V1 receptors, and endothelin via endothelin receptors. The net effect is increased arterial resistance and, in some cases, venous constriction which raises venous return. Local vasoconstrictors may have rapid, short-lived effects suitable for reducing bleeding or nasal congestion, whereas systemic agents are dosed to manage hypotension or shock.

Clinical uses encompass systemic vasopressors for hypotension and shock (for example, norepinephrine, phenylephrine, dopamine, vasopressin, and angiotensin II) and local applications to minimize bleeding during procedures or to treat nasal or ocular congestion. They are also employed in anesthesia to prolong vasoconstriction at the surgical site and in ophthalmology for pupil dilation or redness reduction.

Adverse effects include hypertension, tachycardia, arrhythmias, and reduced tissue perfusion, which can lead to ischemia or necrosis if extravasation occurs. Safety considerations include cardiovascular disease, peripheral vascular disease, pregnancy, and potential drug interactions. Dosing is individualized and requires careful monitoring of blood pressure and perfusion.