Catecholamines: A Major Neurotransmitters- Review for Healthcare Professionals | ||
| Egyptian Journal of Chemistry | ||
| Volume 68, Issue 13, December 2025, Pages 1195-1205 PDF (569.11 K) | ||
| Document Type: Review Articles | ||
| DOI: 10.21608/ejchem.2025.409253.12125 | ||
| Authors | ||
| Abdullah Khatim R. Alanazi; Soliman Mohammed Alehaidib; Maysam Taysir Almegbel; Nasser Ali Alhabib; Mohammed Abdulaziz Almaniea; Amani Ayyadhah Alanazi; Ahlam Mohammed Alzahrani; Rakan Ahmed Albalawi; Mohannad Ali Almusallam; Naif Abdullah M Alanazi; Abdulrahman Rashed Alanazi; Mohammed Ayyat Alanazi; Ibrahim Mohammed Alyamani; Mohammad Hamed Almontashiri; Saud Mohsen Alqurashi; Manal Salem Alsomali; Sami Mallah Alenazi; May Eidhah Almatrafi; Sultan Saad Alharbi | ||
| Ministry of National Guard, Saudi Arabia | ||
| Abstract | ||
| Background: Catecholamines—dopamine, norepinephrine, and epinephrine—are tyrosine-derived messengers that function as neurotransmitters and hormones, synchronizing rapid neuronal communication with systemic endocrine regulation across multiple organ systems. Aim: To synthesize the cellular architecture, receptor pharmacology, organ-system actions, diagnostic strategies, pathophysiology, and therapeutic implications of catecholamine biology for clinicians, drawing on the provided source material. Methods: Narrative integration of evidence summarizing biosynthetic pathways, adrenergic and dopaminergic receptor signaling, systems physiology, related testing (plasma/urine assays, clonidine suppression, DaTscan), disease mechanisms, and clinical interventions. Results: Biosynthesis proceeds from tyrosine, L-DOPA, dopamine, norepinephrine, epinephrine, with vesicular storage, stimulus-coupled exocytosis, transporter-mediated reuptake, and enzymatic degradation (MAO/COMT) ensuring signal fidelity. Catecholamines recalibrate hemodynamics, ventilation, glycemia, motility, perfusion, and behavior across cardiovascular, respiratory, endocrine, gastrointestinal, renal, and neural domains. α1/Gq signaling promotes vasoconstriction, whereas α2/Gi enforces presynaptic and secretory inhibition; β1/β2/β3 receptors couple to Gs–cAMP–PKA to augment cardiac output, bronchodilate, redistribute skeletal-muscle flow, and mobilize lipids. D1-like/D2-like receptors bidirectionally tune motor control, renal perfusion, natriuresis, and neuroendocrine/immune function. Diagnostic evaluation hinges on plasma/urine catecholamines and metanephrines, clonidine suppression to distinguish tumor-driven excess, and DaTscan to visualize nigrostriatal integrity. Disorders include pheochromocytoma/paraganglioma, neurogenic shock, Parkinson disease, heart failure, and catecholamine-induced cardiomyopathy. Therapies span β-blockers, α-blockers, β2-agonists, epinephrine, norepinephrine, dopamine, levodopa, and α2-agonists for hypertension, heart failure, arrhythmias, obstructive lung disease, anaphylaxis, septic shock, movement disorders, and hyperadrenergic states. Conclusion: Catecholamine pathways provide a unifying framework linking cellular chemistry to bedside interventions; receptor-targeted modulation enables amplification of life-preserving responses or attenuation of maladaptive sympathetic drive, improving outcomes across diverse conditions | ||
| Keywords | ||
| Catecholamines; dopamine, norepinephrine, epinephrine, adrenergic receptors, dopamine receptors, Parkinson disease | ||
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