A family of monoamine neurotransmitters and hormones including dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), synthesized from tyrosine via tyrosine hydroxylase. Catecholamines mediate the sympathetic stress response and modulate immune function.
Synthesized via tyrosine β L-DOPA (via tyrosine hydroxylase) β dopamine (via DOPA decarboxylase) β norepinephrine (via dopamine Ξ²-hydroxylase) β epinephrine (via PNMT in adrenal medulla). Released from sympathetic nerve terminals and adrenal medulla during stress. Bind to adrenergic receptors (Ξ±1, Ξ±2, Ξ²1, Ξ²2, Ξ²3) and dopamine receptors (D1-D5) on target tissues including immune cells. Degraded by COMT (catechol-O-methyltransferase) and MAO (monoamine oxidase).
Chronic stress leads to sustained catecholamine elevation, driving hypertension, endothelial dysfunction, oxidative stress, inflammation, insulin resistance, and immune dysregulation. Catecholamines directly modulate immune cell trafficking, cytokine production, and inflammatory responses. COMT polymorphisms (Val158Met) determine catecholamine degradation rates, influencing stress resilience and dopamine availability.
- Include dopamine, norepinephrine, and epinephrine
- Synthesized from tyrosine via tyrosine hydroxylase (rate-limiting step)
- Mediate fight-or-flight response via sympathetic nervous system
- Immune cells express adrenergic and dopamine receptors
- Chronic elevation drives hypertension, insulin resistance, inflammation
- Degraded by COMT and MAO enzymes
- COMT Val158Met polymorphism: Val/Val = high activity (low dopamine), Met/Met = low activity (high dopamine)
- Stress-induced catecholamines suppress cellular immunity (Th1) and enhance humoral immunity (Th2)
- Beta-blockers reduce catecholamine effects on cardiovascular and immune systems
- dopamine β Precursor to norepinephrine and primary catecholamine in reward pathways
- norepinephrine β Synthesized from dopamine, primary sympathetic neurotransmitter
- epinephrine β Synthesized from norepinephrine in adrenal medulla, stress hormone
- tyrosine β Amino acid precursor for all catecholamine synthesis
- COMT β Enzyme degrading catecholamines; polymorphisms affect stress resilience
- sympathetic nervous system β Primary system releasing catecholamines during stress
- HPA axis β Parallel stress axis; cortisol and catecholamines act synergistically
- chronic stress β Causes sustained catecholamine elevation with pathological consequences
- hypertension β Chronic catecholamine elevation increases vascular resistance and blood pressure
- endothelial dysfunction β Catecholamines promote vasoconstriction and oxidative damage to endothelium
- inflammation β Catecholamines can both suppress and promote inflammation depending on receptor type and context
- immune system β Immune cells express catecholamine receptors; modulates trafficking and function
- T cells β Express beta-adrenergic receptors; catecholamines shift Th1/Th2 balance
- macrophages β Express adrenergic receptors; catecholamines modulate polarization
- insulin resistance β Chronic catecholamines impair insulin signaling and promote lipolysis
- oxidative stress β Catecholamine metabolism generates ROS and oxidative damage
- locus coeruleus β Primary source of central norepinephrine release
- prefrontal cortex β Optimal dopamine/norepinephrine levels required for executive function
- quercetin β Inhibits COMT, potentially increasing catecholamine availability
- exercise β Acutely elevates catecholamines for metabolic mobilization
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