Vasoconstrictor agent

Vasoconstrictor agents (also known as vasopressors or pressors) are a functional class of endogenous substances and pharmacological agents that cause the narrowing of blood vessels by inducing the contraction of vascular smooth muscle cells [1, 3]. This physiological process increases systemic vascular resistance and elevates arterial blood pressure, which is essential for maintaining critical organ perfusion during states of shock or severe hypotension [1, 14, 17]. The class encompasses a variety of molecules, including catecholamines like norepinephrine and epinephrine, as well as peptides like angiotensin II, endothelin-1, and vasopressin [2, 3]. In clinical medicine, exogenous vasoconstrictors are widely used to manage hemodynamic instability in intensive care and surgical settings, and are also employed as additives in local anesthetics to reduce regional absorption and prolong anesthetic effect [5, 6]. Their therapeutic use is however associated with significant safety concerns, including the potential for peripheral ischemia, tissue necrosis from extravasation, and increased cardiac afterload that can impair heart function in predisposed patients [1, 5, 14].

Other names

VasoconstrictorVasopressorPressor agentVasoactive agentVasoconstrictive agent

Vasoconstrictor agents produce their effects by binding to specific G protein-coupled receptors (GPCRs) on vascular smooth muscle cells, such as alpha-1 adrenergic, angiotensin II type 1 (AT1), and vasopressin V1 receptors [2, 3]. Activation of these receptors typically triggers a signaling cascade involving the Gq protein and phospholipase C, which produces inositol trisphosphate (IP3) [3]. IP3 promotes the release of calcium from the sarcoplasmic reticulum, leading to an increase in intracellular calcium concentration that activates myosin light chain kinase [1, 3]. This enzyme phosphorylates myosin light chains, enabling actin-myosin interaction and subsequent cellular contraction, which narrows the blood vessel lumen and increases systemic vascular resistance [1, 14].