Physiology, Catecholamines: Stephen Paravati Alan Rosani Steven J. Warrington

Physiology, Catecholamines
Stephen Paravati; Alan Rosani; Steven J. Warrington.

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Last Update: July 26, 2020.
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Introduction
Dopamine, norepinephrine, and epinephrine are physiologically active molecules known as catecholamines. Catecholamines act both as neurotransmitters and
hormones vital to the maintenance of homeostasis through the autonomic nervous system. Physiologic principles of catecholamines have numerous applications
within pharmacology. Pheochromocytoma is a catecholamine-producing neoplasm relevant to clinical medicine.[1][2][3]
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Issues of Concern
The majority of dopamine production occurs in the brain, and the dopaminergic pathways it follows has vast implications on cortical neurophysiology. Dopamine is
chemically classified as a catecholamine, undergoes some synthesis in the adrenal medulla, and has an affinity for adrenergic receptors. However, it is not typically
considered in the context of clinical adrenal physiology to the same level of depth as norepinephrine and epinephrine. Clinically, dopamine has applications for
treating hypotension in patients with shock. It has a particular affinity for receptors located in the renal arteries that, when activated, relax and dilate the renal
vasculature.[4][5][6]
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Cellular
Catecholamine synthesis within the adrenal medulla is controlled by serum concentration of the amino acid tyrosine. Tyrosine undergoes hydroxylation via tyrosine
hydroxylase to form DOPA, which then undergoes decarboxylation to dopamine. Dopamine may be secreted into the bloodstream or undergo further hydroxylation to
norepinephrine (noradrenaline). Norepinephrine can be secreted into the bloodstream or further modified by a methyltransferase to epinephrine (adrenaline) and then
secreted. Glucocorticoids notably upregulate methyltransferase activity to increase epinephrine production. Degradation of catecholamines to their metabolites occurs
either by monoamine oxidase (MAO) located in the outer mitochondrial membrane of the cell and/or by catechol-o-methyltransferase (COMT) found within the
cytosol of the cell. MAO and COMT catabolize norepinephrine and epinephrine to vanillylmandelic acid (VMA), and dopamine to homovanillic acid (HVA). VMA
and HVA are excreted in urine.[7][8][9]
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Development
In early fetal development, ventral migration of neural crest cells from the neuroectoderm coalesce form a sympathetic ganglion. Some of these neural crest cells
migrate further from the sympathetic ganglion and are subsequently enveloped by mesenchymal cells of the developing fetal adrenal cortex. The surrounded neural
crest cells become the adrenal medulla. These cells develop into chromaffin cells capable of synthesizing catecholamines.
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Organ Systems Involved
Neuroendocrine chromaffin cells, responsible for the biosynthesis of catecholamines, are located throughout the brain and in the adrenal glands. The highest density of
chromaffin cells is located within the adrenal medulla, the most functionally significant area of catecholamine production. The kidneys are responsible for excreting
the byproducts of catecholamine degradation. Adrenergic receptors activated by catecholamines are located in multisystem smooth muscle and adipose tissue.
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Function
The “fight or flight” response of the sympathetic nervous system is a direct result of the multisystem action of catecholamines. Secretion from the adrenal medulla
proceeding the activation of the sympathetic nervous system functions to regulate blood pressure by contracting the smooth muscle in the vasculature (via alpha-1
receptors). The adrenergic receptors linked to blood vessels have an especially high affinity for norepinephrine relative to the other amines. Further musculoskeletal
actions of catecholamines include enhanced contractility of cardiac muscle (via beta-1 receptors), contraction of the pupillary dilator (via alpha-1 receptors),
piloerection (via alpha-1 receptors), and relaxation of smooth muscle in the gastrointestinal tract, urinary tract, and bronchioles (via beta-2 receptors). Both
epinephrine and norepinephrine modulate metabolism to increase blood glucose levels by stimulating glycogenolysis in the liver (via beta-2 receptors), increased
glucagon secretion (via beta-2 receptors) and decreased insulin secretion (via alpha-2 receptors) from the pancreas, and lipolysis in adipose tissue (via beta-3
receptors). Epinephrine also inhibits release of mediators from mast cells and basophils in type I hypersensitivity reactions.

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Physiology, Catecholamines

Stephen Paravati; Alan Rosani; Steven J. Warrington.

Last Update: July 26, 2020.

Organ Systems Involved

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