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Sympathetic nervous system
Sympathetic nervous system
Sympathetic nervous system
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Sympathetic nervous system
Schematic illustration showing the sympathetic nervous system with sympathetic cord and target organs.
Details
Identifiers
Latinpars sympathica divisionis autonomici systematis nervosi
AcronymSNS or SANS
MeSHD013564
TA98A14.3.01.001
TA26601
FMA9906
Anatomical terminology

The sympathetic nervous system (SNS; or sympathetic autonomic nervous system, SANS, to differentiate it from the somatic nervous system) is one of the three divisions of the autonomic nervous system, the others being the parasympathetic nervous system and the enteric nervous system.[1][2] The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system.[3]

The autonomic nervous system functions to regulate the body's unconscious actions. The sympathetic nervous system's primary process is to stimulate the body's fight or flight response. It is, however, constantly active at a basic level to maintain homeostasis.[4] The sympathetic nervous system is described as being antagonistic to the parasympathetic nervous system. The latter stimulates the body to "feed and breed" and to (then) "rest-and-digest".

The SNS has a major role in various physiological processes such as blood glucose levels, body temperature, cardiac output, and immune system function. The formation of sympathetic neurons being observed at embryonic stage of life and its development during aging shows its significance in health; its dysfunction has shown to be linked to various health disorders.[5]

Structure

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There are two kinds of neurons involved in the transmission of any signal through the sympathetic system: pre-ganglionic and post-ganglionic. The shorter preganglionic neurons originate in the thoracolumbar division of the spinal cord specifically at T1 to L2~L3, and travel to a ganglion, often one of the paravertebral ganglia, where they synapse with a postganglionic neuron. From there, the long postganglionic neurons extend across most of the body.[6]

At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons. In response to this stimulus, the postganglionic neurons release norepinephrine, which activates adrenergic receptors that are present on the peripheral target tissues. The activation of target tissue receptors causes the effects associated with the sympathetic system. However, there are three important exceptions:[7]

  1. Postganglionic neurons of sweat glands release acetylcholine for the activation of muscarinic receptors, except for areas of thick skin, the palms and the plantar surfaces of the feet, where norepinephrine is released and acts on adrenergic receptors. This leads to the activation of sudomotor function, which is assessed by electrochemical skin conductance.
  2. Chromaffin cells of the adrenal medulla are analogous to post-ganglionic neurons; the adrenal medulla develops in tandem with the sympathetic nervous system and acts as a modified sympathetic ganglion. Within this endocrine gland, pre-ganglionic neurons synapse with chromaffin cells, triggering the release of two transmitters: a small proportion of norepinephrine, and more substantially, epinephrine. The synthesis and release of epinephrine as opposed to norepinephrine is another distinguishing feature of chromaffin cells compared to postganglionic sympathetic neurons.[8]
  3. Postganglionic sympathetic nerves terminating in the kidney release dopamine, which acts on dopamine D1 receptors of blood vessels to control how much blood the kidney filters. Dopamine is the immediate metabolic precursor to norepinephrine, but is nonetheless a distinct signaling molecule.[9]

Organization

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The sympathetic nervous system extends from the thoracic to lumbar vertebrae and has connections with the thoracic, abdominal, and pelvic plexuses.

Sympathetic nerves arise from near the middle of the spinal cord in the intermediolateral nucleus of the lateral grey column, beginning at the first thoracic vertebra of the vertebral column and are thought to extend to the second or third lumbar vertebra. Because its cells begin in the thoracolumbar division – the thoracic and lumbar regions of the spinal cord – the sympathetic nervous system is said to have a thoracolumbar outflow. Axons of these nerves leave the spinal cord through the anterior root. They pass near the spinal (sensory) ganglion, where they enter the anterior rami of the spinal nerves. However, unlike somatic innervation, they quickly separate out through white rami connectors (so called from the shiny white sheaths of myelin around each axon) that connect to either the paravertebral (which lie near the vertebral column) or prevertebral (which lie near the aortic bifurcation) ganglia extending alongside the spinal column.

To reach target organs and glands, the axons must travel long distances in the body, and, to accomplish this, many axons relay their message to a second cell through synaptic transmission. The ends of the axons link across a space, the synapse, to the dendrites of the second cell. The first cell (the presynaptic cell) sends a neurotransmitter across the synaptic cleft, where it activates the second cell (the postsynaptic cell). The message is then carried to the final destination.

Scheme showing structure of a typical spinal nerve. 1. Somatic efferent. 2. Somatic afferent. 3,4,5. Sympathetic efferent. 6,7. Sympathetic afferent.

Presynaptic nerves' axons terminate in either the paravertebral ganglia or prevertebral ganglia. There are four different paths an axon can take before reaching its terminal. In all cases, the axon enters the paravertebral ganglion at the level of its originating spinal nerve. After this, it can then either synapse in this ganglion, ascend to a more superior or descend to a more inferior paravertebral ganglion and synapse there, or it can descend to a prevertebral ganglion and synapse there with the postsynaptic cell.[10]

The postsynaptic cell then goes on to innervate the targeted end effector (i.e. gland, smooth muscle, etc.). Because paravertebral and prevertebral ganglia are close to the spinal cord, presynaptic neurons are much shorter than their postsynaptic counterparts, which must extend throughout the body to reach their destinations.

A notable exception to the routes mentioned above is the sympathetic innervation of the suprarenal (adrenal) medulla. In this case, presynaptic neurons pass through paravertebral ganglia, on through prevertebral ganglia and then synapse directly with suprarenal tissue. This tissue consists of cells that have pseudo-neuron like qualities in that when activated by the presynaptic neuron, they will release their neurotransmitter (epinephrine) directly into the bloodstream.

In the sympathetic nervous system and other peripheral nervous system components, these synapses are made at sites called ganglia. The cell that sends its fiber is called a preganglionic cell, while the cell whose fiber leaves the ganglion is called a postganglionic cell. As mentioned previously, the preganglionic cells of the sympathetic nervous system are located between the first thoracic segment and the third lumbar segments of the spinal cord. Postganglionic cells have their cell bodies in the ganglia and send their axons to target organs or glands.

The ganglia include not just the sympathetic trunks but also the cervical ganglia (superior, middle and inferior), which send sympathetic nerve fibers to the head and thorax organs, and the celiac and mesenteric ganglia, which send sympathetic fibers to the gut.


Autonomic nervous system's jurisdiction to organs in the human body edit
Organ Nerves[11] Spinal column origin[11]
stomach T5, T6, T7, T8, T9, sometimes T10
duodenum T5, T6, T7, T8, T9, sometimes T10
jejunum and ileum T5, T6, T7, T8, T9
spleen T6, T7, T8
gallbladder and liver T6, T7, T8, T9
colon
pancreatic head T8, T9
appendix T10
bladder S2-S4
kidneys and ureters T11, T12

Information transmission

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Sympathetic nervous system – Information transmits through it affecting various organs.

Messages travel through the sympathetic nervous system in a bi-directional flow. Efferent messages can simultaneously trigger changes in different body parts. For example, the sympathetic nervous system can accelerate heart rate; widen bronchial passages; decrease motility (movement) of the large intestine; constrict blood vessels; increase peristalsis in the oesophagus; cause pupillary dilation, piloerection (goose bumps) and perspiration (sweating); and raise blood pressure. One exception is with certain blood vessels, such as those in the cerebral and coronary arteries, which dilate (rather than constrict) with increased sympathetic tone. This is because of a proportional increase in the presence of β2 adrenergic receptors rather than α1 receptors. β2 receptors promote vessel dilation instead of constriction like α1 receptors. An alternative explanation is that the primary (and direct) effect of sympathetic stimulation on coronary arteries is vasoconstriction followed by a secondary vasodilation caused by the release of vasodilatory metabolites due to the sympathetically increased cardiac inotropy and heart rate. This secondary vasodilation caused by the primary vasoconstriction is termed functional sympatholysis, the overall effect of which on coronary arteries is dilation.[12] The target synapse of the postganglionic neuron is mediated by adrenergic receptors and is activated by either norepinephrine (noradrenaline) or epinephrine (adrenaline).

Function

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Examples of sympathetic system action on various organs[8] except where otherwise indicated.
Organ Effect
Eye Dilates pupil
Heart Increases rate and force of contraction
Lungs Dilates bronchioles via circulating adrenaline[13]
Blood vessels Dilates in skeletal muscle[14]
Constricts in gastrointestinal organs
Sweat glands Activates sudomotor function and sweat secretion
Digestive tract Inhibits peristalsis
Kidney Increases renin secretion
Penis Doesn't cause erection
Ductus deferens Promotes emission prior to ejaculation

The sympathetic nervous system is responsible for up- and down-regulating many homeostatic mechanisms in living organisms. Fibers from the SNS innervate tissues in almost every organ system, providing at least some regulation of functions as diverse as pupil diameter, gut motility, and urinary system output and function.[15] It is perhaps best known for mediating the neuronal and hormonal stress response commonly known as the fight-or-flight response. This response is also known as sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla (but also all other sympathetic fibers) secrete acetylcholine, which activates the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it. Therefore, this response that acts primarily on the cardiovascular system is mediated directly via impulses transmitted through the sympathetic nervous system and indirectly via catecholamines secreted from the adrenal medulla.

The sympathetic nervous system is responsible for priming the body for action, particularly in situations threatening survival.[16] One example of this priming is in the moments before waking, in which sympathetic outflow spontaneously increases in preparation for action.

Sympathetic nervous system stimulation causes vasoconstriction of most blood vessels, including many of those in the skin, the digestive tract, and the kidneys. This occurs due to the activation of alpha-1 adrenergic receptors by norepinephrine released by post-ganglionic sympathetic neurons. These receptors exist throughout the vasculature of the body but are inhibited and counterbalanced by beta-2 adrenergic receptors (stimulated by epinephrine release from the adrenal glands) in the skeletal muscles, the heart, the lungs, and the brain during a sympathoadrenal response. The net effect of this is a shunting of blood away from the organs not necessary to the immediate survival of the organism and an increase in blood flow to those organs involved in intense physical activity.

Sensation

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The afferent fibers of the autonomic nervous system, which transmit sensory information from the internal organs of the body back to the central nervous system (or CNS), are not divided into parasympathetic and sympathetic fibers as the efferent fibers are.[17] Instead, autonomic sensory information is conducted by general visceral afferent fibers.

General visceral afferent sensations are mostly unconscious visceral motor reflex sensations from hollow organs and glands that are transmitted to the CNS. While the unconscious reflex arcs normally are undetectable, in certain instances they may send pain sensations to the CNS masked as referred pain. If the peritoneal cavity becomes inflamed or if the intestine is suddenly distended, the body will interpret the afferent pain stimulus as somatic in origin. This pain is usually non-localized. The pain is also usually referred to dermatomes that are at the same spinal nerve level as the visceral afferent synapse.[citation needed]

Relationship with the parasympathetic nervous system

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Together with the other component of the autonomic nervous system, the parasympathetic nervous system, the sympathetic nervous system aids in the control of most of the body's internal organs. Reaction to stress—as in the flight-or-fight response—is thought to be elicited by the sympathetic nervous system and to counteract the parasympathetic system, which works to promote maintenance of the body at rest. The comprehensive functions of both the parasympathetic and sympathetic nervous systems are not so straightforward, but this is a useful rule of thumb.[4][18]

Origins

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It was originally believed that the sympathetic nervous system arose with jawed vertebrates.[19] However, the sea lamprey (Petromyzon marinus), a jawless vertebrate, has been found to contain the key building blocks and developmental controls of a sympathetic nervous system.[20] Nature described this research as a "landmark study" that "point to a remarkable diversification of sympathetic neuron populations among vertebrate classes and species".[21]

Disorders

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The dysfunction of the sympathetic nervous system is linked to many health disorders, such as heart failure, gastrointestinal problems and immune dysfunction, as well as metabolic disorders like hypertension and diabetes, highlighting the importance of the sympathetic nervous system for health.

The sympathetic stimulation of metabolic tissues is required for the maintenance of metabolic regulation and feedback loops. The dysregulation of this system leads to an increased risk of neuropathy within metabolic tissues and therefore can worsen or precipitate metabolic disorders. An example of this includes the retraction of sympathetic neurons due to leptin resistance, which is linked to obesity.[22] Another example, although more research is required, is the observed link that diabetes results in the impairment of synaptic transmission due to the inhibition of acetylcholine receptors as a result of high blood glucose levels. The loss of sympathetic neurons is also associated with the reduction of insulin secretion and impaired glucose tolerance, further exacerbating the disorder.[23]

The sympathetic nervous system holds a major role in long-term regulation of hypertension, whereby the central nervous system stimulates sympathetic nerve activity in specific target organs or tissues via neurohumoral signals. In terms of hypertension, the overactivation of the sympathetic system results in vasoconstriction and increased heart rate resulting in increased blood pressure. In turn, increasing the potential of the development of cardiovascular disease.[24]

In heart failure, the sympathetic nervous system increases its activity, leading to increased force of muscular contractions that in turn increases the stroke volume, as well as peripheral vasoconstriction to maintain blood pressure. However, these effects accelerate disease progression, eventually increasing mortality in heart failure.[25]

Sympathicotonia is a stimulated condition of the sympathetic nervous system, marked by vascular spasm elevated blood pressure, and goose bumps.[26][27]

Heightened sympathetic nervous system activity is also linked to various mental health disorders such as, anxiety disorders and post-traumatic stress disorder (PTSD). It is suggested that the overactivation of the SNS results in the increased severity of PTSD symptoms. In accordance with disorders like hypertension and cardiovascular disease mentioned above, PTSD is also linked with the increased risk of developing mentioned diseases, further correlating the link between these disorders and the SNS.[28]

The sympathetic nervous system is sensitive to stress, studies suggest that the chronic dysfunction of the sympathetic system results in migraines, due to the vascular changes associated with tension headaches. Individuals with migraine attacks are exhibited to have symptoms that are associated with sympathetic dysfunction, which include reduced levels of plasma norepinephrine levels, sensitivity of the peripheral adrenergic receptors.[29]

Insomnia is a sleeping disorder, that makes falling or staying asleep difficult, this disruption in sleep results in sleep deprivation and various symptoms, with the severity depending on whether the insomnia is acute or chronic. The most favoured hypothesis for the cause of insomnia is the hyperarousal hypothesis, which is known as a collective over-activation of various systems in the body, this over-activation includes the hyperactivity of the SNS. Whereby during sleep cycle disruption sympathetic baroreflex function and neural cardiovascular responses become impaired.[30][31]

However more research is still required, as methods used in measuring SNS biological measures are not so reliable due to the sensitivity of the SNS. Many factors easily affect its activity, like stress, environment, timing of day, and disease. These factors can impact results significantly and for more accurate results extremely invasive methods are required, such as microneurography. The difficulty of measuring the SNS activity does not only apply to insomnia, but also with various disorders previously discussed. However, over time with advancements in technology and techniques in research studies the disruption of the SNS and its impact on the human body will be explored further. [32][33]

History and etymology

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The name of this system can be traced to the concept of sympathy, in the sense of "connection between parts", first used medically by Galen.[34] In the 18th century, Jacob B. Winslow applied the term specifically to nerves.[35]

The concept that an independent part of the nervous system coordinates body functions had its origin in the works of Galen (129–199), who proposed that nerves distributed spirits throughout the body. From animal dissections he concluded that there were extensive interconnections from the spinal cord to the viscera and from one organ to another. He proposed that this system fostered a concerted action or 'sympathy' of the organs. Little changed until the Renaissance when Bartolomeo Eustacheo (1545) depicted the sympathetic nerves, the vagus and adrenal glands in anatomical drawings. Jacobus Winslow (1669–1760), a Danish-born professor working in Paris, popularised the term 'sympathetic nervous system' in 1732 to describe the chain of ganglia and nerves which were connected to the thoracic and lumbar spinal cord.[36]

See also

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References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Sympathetic nervous system

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from Grokipedia
The sympathetic nervous system (SNS) is one of the two primary divisions of the , responsible for mediating the body's involuntary " to stress, danger, or physical demands. This response mobilizes energy resources by accelerating heart rate, enhancing flow to skeletal muscles, dilating airways for improved oxygenation, and suppressing non-essential functions like . Overall, the SNS prepares the for immediate action, contrasting with the parasympathetic nervous system's role in "rest and digest" activities to maintain . Anatomically, the SNS originates from the thoracolumbar (T1-L2) segments of the , where preganglionic neurons arise from the intermediolateral cell column in the lateral horn. These short preganglionic fibers with longer postganglionic neurons primarily in paravertebral chain ganglia (along the spinal column) or prevertebral ganglia (near abdominal organs). The SNS also includes the , which functions as a modified postganglionic , releasing hormones directly into the bloodstream upon . This decentralized allows for widespread, coordinated innervation of target organs throughout the body. Functionally, the SNS transmits signals via a two-neuron chain: preganglionic neurons release to activate nicotinic receptors on postganglionic neurons, while postganglionic neurons primarily release norepinephrine (or epinephrine in the ) to bind adrenergic receptors (alpha-1, alpha-2, beta-1, beta-2) on effector tissues. An exception occurs in sweat glands and arrector pili muscles, where postganglionic fibers use on muscarinic receptors. These neurotransmitters enable diverse effects, such as increasing and contractility (beta-1 receptors), promoting bronchodilation and in (beta-2 receptors), and inducing in the skin and viscera (alpha-1 receptors). The SNS exerts profound influences across multiple organ systems to support survival under stress. In the cardiovascular system, it elevates and while redirecting perfusion to vital areas. Respiratory effects include pupil dilation for enhanced vision and airway expansion for better . Metabolically, it stimulates and to provide rapid energy, inhibits gastrointestinal and to conserve resources, and promotes sweating for . Dysregulation of the SNS is implicated in conditions like and anxiety disorders, underscoring its role in both acute responses and chronic health.

Anatomy

Organization

The sympathetic nervous system (SNS) exhibits a two-neuron chain in its efferent pathway, consisting of preganglionic and postganglionic neurons. Preganglionic neurons originate from the intermediolateral cell column of the 's gray matter in the thoracolumbar region, specifically segments T1 through L2 or L3. These neurons send myelinated preganglionic axons that exit the via the ventral roots, pass through the spinal nerves (T1-L2/L3), and enter the sympathetic chain ganglia via the white rami communicantes, where they synapse with postganglionic neurons. Postganglionic neurons, located in paravertebral or prevertebral ganglia, extend unmyelinated axons to target organs, enabling widespread innervation. The primary anatomical framework of the SNS is the , a paired chain of interconnected ganglia that extends longitudinally along the vertebral column from the to the . This trunk is divided into cervical, thoracic, , and sacral segments. The cervical portion typically includes three ganglia: the (at C1-C3 level), middle cervical ganglion (at C5-C6), and inferior cervical ganglion (often fused with the first thoracic ganglion to form the at C7-T1). The thoracic segment features 10 to 12 ganglia, the segment 4 ganglia, the sacral segment 4 to 5 ganglia, and a small unpaired coccygeal ganglion where the chains converge. Paravertebral ganglia in the trunk receive preganglionic inputs and distribute postganglionic fibers to nearby structures, while prevertebral ganglia, located anterior to the vertebral column in the , handle visceral innervation. Splanchnic nerves represent specialized preganglionic pathways that bypass the paravertebral ganglia to innervate abdominal organs. The greater arises from T5 to T9 segments, the lesser from T10 to T11, and the least (or lowest) from T12; these nerves pierce the crus of the diaphragm and primarily in the celiac, superior mesenteric, and aorticorenal prevertebral ganglia. From these sites, postganglionic fibers supply sympathetic innervation to the , , and derivatives, including the , intestines, liver, and . splanchnic nerves (from L1-L2) contribute similarly to pelvic organs via the inferior mesenteric and hypogastric ganglia. Distinct pathways within the SNS include cardiac accelerator nerves and vasomotor nerves. Cardiac accelerator nerves originate as preganglionic fibers from the upper thoracic segments (T1-T4), ascend the sympathetic trunk to synapse in the cervical ganglia, and convey postganglionic fibers to the heart via the cardiac plexus to modulate rate and contractility. Vasomotor nerves, primarily postganglionic, arise from various trunk levels and innervate vascular smooth muscle throughout the body, facilitating vasoconstriction in skin, viscera, and skeletal muscle. A hallmark of SNS organization is the divergence of preganglionic fibers, allowing amplification of signals for coordinated responses; a single preganglionic may synapse with 10 to 20 or more postganglionic neurons in the ganglia, compared to the more discrete 1:1 to 1:4 ratio in the parasympathetic system. This divergence, facilitated by branching within the ganglia, enables one central command to influence multiple effectors simultaneously.

Information transmission

The sympathetic nervous system's information transmission begins at the preganglionic level, where neurons originating in the intermediolateral cell column of the (thoracolumbar segments T1 to L2) release as the primary . This binds to nicotinic acetylcholine receptors on the postganglionic neurons within the , facilitating rapid excitatory transmission via ligand-gated ion channels that depolarize the postsynaptic membrane. These nicotinic receptors are pentameric ion channels permeable to sodium and , ensuring fast synaptic activation essential for coordinating autonomic responses. Postganglionic neurons, in turn, primarily employ norepinephrine as their , classifying most sympathetic transmission as adrenergic. Norepinephrine is released from varicosities—swellings along the unmyelinated postganglionic axons—into the neuroeffector junctions, where it diffuses to target tissues rather than forming discrete synapses. An exception occurs in sympathetic innervation of sweat glands and some vasodilator fibers, where serves as the postganglionic , acting on muscarinic receptors to elicit responses. Norepinephrine primarily interacts with adrenergic receptors, which are G-protein-coupled receptors divided into alpha and beta subtypes. Alpha-1 receptors (α1), coupled to proteins, activate the pathway via IP3 and Ca²⁺ signaling, and are predominantly located on vascular cells to mediate . Alpha-2 receptors (α2), linked to Gi proteins, inhibit to decrease cAMP levels and are found presynaptically on postganglionic neurons for feedback inhibition of norepinephrine release, as well as on some vascular sites. Beta-1 receptors (β1), coupled to Gs proteins, stimulate to increase cAMP and are mainly expressed in cardiac tissue to enhance and contractility. Beta-2 receptors (β2), also Gs-coupled, promote bronchodilation and vascular relaxation and are located in the lungs, blood vessels, and . Beta-3 receptors (β3), Gs-coupled like β1 and β2, are primarily in to facilitate . Several neuromodulators enhance or modulate sympathetic transmission alongside norepinephrine. , as a biosynthetic precursor to norepinephrine, can be co-released from sympathetic terminals and acts via to influence vascular tone and immune responses in peripheral tissues. (NPY) is co-stored and released from large dense-core vesicles in postganglionic neurons, exerting prejunctional inhibition of norepinephrine and ATP release while potentiating postjunctional vasoconstrictive effects through Y1 receptors on . (ATP) is co-released with norepinephrine from small synaptic vesicles, binding to P2X ionotropic receptors for rapid excitatory effects on and contributing to the initial phase of sympathetic responses before norepinephrine's slower actions dominate. Synaptic processes in the sympathetic nervous system involve distinct structures for efficient propagation. Preganglionic-postganglionic communication occurs at chemical synapses within paravertebral or prevertebral ganglia, where acetylcholine release into the synaptic cleft triggers precise, point-to-point transmission via nicotinic receptors. In contrast, postganglionic transmission employs varicosities, which lack traditional synaptic specializations and release norepinephrine (and co-transmitters) diffusely into the surrounding effector cells, allowing for volume transmission that integrates signals across broader tissue areas. This diffuse release mechanism supports the sympathetic system's role in widespread, coordinated activation.

Physiology

Fight-or-flight response

The represents the acute activation of the sympathetic nervous system in reaction to perceived threats, mobilizing the body for immediate action through coordinated physiological changes. This response, first conceptualized by Walter Cannon in the early , integrates sensory inputs to prepare for survival by enhancing energy availability and sensory acuity while suppressing non-essential functions. Trigger mechanisms begin with integration, primarily involving the , which coordinates stress signals via the sympathetic-adreno-medullary (SAM) axis. The , a key noradrenergic nucleus in the , amplifies arousal by projecting to the and , facilitating rapid neural outflow from the spinal cord's intermediolateral cell column to sympathetic preganglionic neurons. This outflow releases norepinephrine at postganglionic synapses, directly innervating target organs. Core effects include , where sympathetic stimulation increases and contractility to boost ; , dilating pupils for improved ; bronchodilation, expanding airways to enhance oxygen uptake; and in the liver and skeletal muscles, rapidly elevating blood glucose for energy mobilization. These changes occur alongside in non-essential areas and redirection of blood flow to vital organs. The hormonal arm amplifies these effects through the , which secretes approximately 80% epinephrine and 20% norepinephrine into the bloodstream, binding to adrenergic receptors body-wide for broader, sustained influence. In contrast, the neural arm provides direct, localized innervation for faster, targeted responses. The neural component onset is nearly instantaneous, within seconds, while the hormonal effects build over minutes and persist longer, ensuring prolonged readiness.

Organ-specific effects

The sympathetic nervous system exerts diverse effects on the cardiovascular system through adrenergic receptors, primarily increasing and contractility via β1 receptors on cardiac myocytes, which enhances myocardial force and conduction velocity. In vascular beds, α1 receptors mediate in the skin and , redirecting blood flow to vital organs during stress, while β2 receptors promote in and , improving oxygen delivery to active tissues. Sympathetic activation on the induces bronchodilation primarily through β2 adrenergic receptors on bronchial , reducing and facilitating increased airflow during heightened demand. This effect is mediated by norepinephrine release from postganglionic fibers, optimizing without altering respiratory directly. In the gastrointestinal system, sympathetic innervation inhibits motility and secretion via α2 and β2 receptors on enteric neurons and , decreasing and promoting contraction to conserve and redirect resources. Norepinephrine acts presynaptically to suppress release from parasympathetic terminals, further dampening digestive processes, while postganglionic fibers in prevertebral ganglia provide tonic to reduce blood flow. Additionally, circulating epinephrine (adrenaline) released from the adrenal medulla decreases gut smooth muscle contraction by causing relaxation primarily via β2-adrenergic receptors, further contributing to sympathetic inhibition of gastrointestinal motility and reducing contraction force and frequency. The receives sympathetic input that facilitates in males by contracting the neck and seminal vesicle through α1 receptors, ensuring retrograde prevention during emission. In the , sympathetic via α1 receptors causes internal contraction and detrusor relaxation, promoting storage, while activation coordinates these responses for continence. Metabolically, sympathetic stimulate in primarily via β3 adrenergic receptors, mobilizing free fatty acids for energy utilization during catabolic states. In the kidneys, β1 receptors on juxtaglomerular cells trigger renin release, activating the renin-angiotensin-aldosterone system to support and . An exception occurs in eccrine sweat glands, where sympathetic innervation is and muscarinic, promoting thermoregulatory sweating independent of adrenergic pathways.

Relationship with parasympathetic nervous system

The sympathetic and parasympathetic nervous systems represent the two primary divisions of the autonomic nervous system, characterized by distinct anatomical outflows that enable their complementary roles in regulating visceral functions. The sympathetic division originates from the thoracolumbar region of the spinal cord, specifically segments T1 to L2, where preganglionic neurons are located in the intermediolateral cell column, leading to shorter preganglionic fibers and ganglia positioned near the spinal cord, such as the paravertebral chain. In contrast, the parasympathetic division arises from the craniosacral outflow, with preganglionic neurons in brainstem nuclei associated with cranial nerves III, VII, IX, and X, as well as sacral segments S2 to S4, resulting in longer preganglionic fibers and ganglia situated close to or within target organs. These structural differences facilitate the sympathetic system's broader, more diffuse activation during stress, while the parasympathetic system allows for more localized, precise control during maintenance activities. Functionally, the two systems often exhibit antagonism, where sympathetic promotes excitatory effects to prepare the body for immediate action, and parasympathetic input provides inhibitory counterbalance to conserve energy. For instance, in the heart, sympathetic stimulation via β-adrenergic receptors increases () and contractility, whereas parasympathetic through muscarinic receptors slows () and reduces conduction velocity. Similar opposition occurs in the lungs, with sympathetic β2 receptor-mediated bronchodilation enhancing airflow, opposed by parasympathetic M3 receptor-induced that maintains baseline tone. In the , sympathetic α1, α2, and β1 receptor effects decrease motility and promote sphincter contraction to inhibit , while parasympathetic M3 receptor stimulation increases secretory activity and to facilitate nutrient absorption. This reciprocal interplay ensures dynamic adjustment of organ function based on physiological demands. Most visceral organs receive dual innervation from both systems, allowing for fine-tuned regulation through their opposing influences, though notable exceptions exist that highlight specialized adaptations. Organs such as the heart, lungs, and gastrointestinal tract exemplify this dual pattern, where the balance between sympathetic and parasympathetic inputs determines net activity, such as modulating cardiac output or digestive efficiency. However, the adrenal medulla receives sympathetic innervation exclusively, with preganglionic fibers directly synapsing on chromaffin cells to release catecholamines into the bloodstream, bypassing traditional postganglionic neurons. Likewise, blood vessels in skeletal muscle lack parasympathetic supply and are controlled solely by sympathetic vasomotor fibers, enabling rapid adjustments in blood flow during physical exertion without counteractive inhibition. These patterns underscore the autonomic system's flexibility in supporting both widespread mobilization and targeted homeostasis. Central integration of the sympathetic and parasympathetic systems occurs primarily through and structures, which coordinate their outputs to maintain overall . The , particularly the paraventricular nucleus, serves as a key integrator, projecting to preganglionic neurons in the (e.g., dorsal motor nucleus of the vagus for parasympathetic) and spinal cord intermediolateral columns (for sympathetic), while receiving sensory feedback via the nucleus of the solitary tract. nuclei, including those in the , further refine this control through reflex loops that adjust autonomic tone in response to visceral afferents, ensuring balanced regulation of functions like and respiration. This allows for seamless transitions between sympathetic dominance and parasympathetic prevalence, adapting to environmental or internal changes. The interplay between these systems embodies the classic "fight-or-flight" versus "rest-and-digest" , an evolutionary that optimizes survival by prioritizing energy allocation. The sympathetic-driven evolved as a rapid survival mechanism in ancestral environments, mobilizing resources—such as increased and redirected blood flow—to confront or evade threats like predators, typically lasting only minutes to prevent resource depletion. Conversely, the parasympathetic rest-and-digest mode activates post-threat to restore equilibrium, promoting , immune recovery, and , which was crucial for long-term viability after escaping danger, as seen in how prey animals quickly shift to relaxation upon safety. This dual framework, rooted in the need to alternate between acute defense and sustained maintenance, reflects the autonomic system's role in evolutionary fitness by balancing immediate reactivity with recuperative processes.

Development

Embryonic origins

The sympathetic nervous system originates during early embryogenesis from cells of the and the . Neural crest cells, which arise from the dorsal aspect of the closing , give rise to the postganglionic neurons and associated structures of the sympathetic division. Specifically, the sympathoadrenal lineage emerges from trunk-level cells, corresponding to levels approximately 6 through 28, which contribute to the formation of along the thoracic and upper regions. These cells undergo epithelial-to-mesenchymal transition and migrate ventrolaterally through the rostral halves of the , avoiding the caudal sclerotome due to inhibitory signals like ephrins, to reach their destinations near the dorsal aorta. Differentiation of sympathetic components involves distinct progenitors for preganglionic and postganglionic neurons. Preganglionic sympathetic neurons develop from neuroblasts in the ventral , specifically within the intermediolateral cell column of the thoracic and upper lumbar segments (T1-L2/L3), emerging as the differentiates into basal plate derivatives under the influence of sonic hedgehog signaling from the and floor plate. In contrast, postganglionic neurons differentiate from migrating cells that aggregate near the dorsal aorta, where local environmental cues promote their commitment to a noradrenergic . The , a key sympathetic effector, forms from chromaffin cells derived from the same sympathoadrenal progenitors as postganglionic neurons; these cells migrate into the developing primordium and differentiate into epinephrine- or norepinephrine-secreting cells, influenced by glucocorticoids from the that suppress neuronal traits and promote endocrine function. Genetic regulation plays a critical role in establishing segmental identity and sympathetic specification. Hox genes, particularly those in the HoxB cluster such as HoxB8, confer rostrocaudal patterning to neural crest derivatives, ensuring appropriate positioning of sympathetic ganglia along the body axis by interacting with neural crest transcription factors like Phox2b. Bone morphogenetic protein (BMP) signaling, emanating from the dorsal aorta (via BMP2, BMP4, and BMP7), is essential for inducing sympathetic neurogenesis from neural crest precursors through both Smad4-dependent transcriptional activation and Smad-independent pathways that promote neuronal survival and differentiation. Disruption of BMP signaling, as shown in conditional knockouts, severely impairs sympathetic ganglion formation. In human embryos, this developmental sequence follows a precise timeline. Initial delamination and migration begin around the fourth week post-fertilization (approximately 22-28 days), coinciding with closure. By the early fifth week (Carnegie Stage [CS] 14, ~33 days), clusters of ganglionic cells from aggregates become identifiable lateral to the dorsal in the cervical and upper thoracic regions. proper form by the eighth week (~56 days, CS23), organizing into paravertebral chains with a characteristic "pearls-on-a-string" arrangement of cell clusters connected by nerve fibers, while prevertebral plexuses emerge concurrently in abdominal regions.

Anatomical maturation

The sympathetic nervous system undergoes significant postnatal growth, adapting to the expanding body size and increasing functional demands. The paravertebral sympathetic chain elongates in parallel with spinal column growth during childhood, ensuring proper alignment and coverage along the vertebral axis. Innervation density in target organs increases progressively; for instance, in skeletal muscles such as the extensor digitorum longus, sympathetic fibers innervating neuromuscular junctions rise from approximately 40% at birth to over 90% in adulthood, as marked by expression. Similarly, in the cardiovascular system, sympathetic axons extend from the stellate ganglia into the myocardium, with density peaking in subepicardial regions and conduction nodes during early postnatal periods, driven by like (NGF). This maturation establishes baseline autonomic control, with critical periods in —particularly the first few postnatal weeks in , equivalent to infancy in humans—essential for cardiovascular innervation establishment, where disruptions like NGF deprivation can reduce volume by up to 80% and lead to neuronal loss. Plasticity remains a hallmark of the sympathetic nervous system throughout life, allowing adaptive responses to physiological changes and injuries. In response to or injury, such as lesions, surviving preganglionic axons sprout extensively within paravertebral ganglia, forming new synaptic connections; for example, after partial , up to 70% of postganglionic neurons develop strong inputs within 4–5 weeks, potentially altering vascular tone. During , hormonal shifts, particularly , drive remodeling of sympathetic innervation in reproductive organs; in the , nerve density decreases markedly at the onset of estrus due to axonal degeneration mediated by , while overall genital innervation matures to support functions like emission and detumescence. Environmental factors further influence this plasticity: regular exercise enhances sympathetic tone by increasing muscle sympathetic nerve activity and improving neurovascular coupling during development and adulthood, promoting adaptive cardiovascular responses. Nutritional status also plays a role, with early postnatal low-protein diets altering autonomic in adulthood, including heightened sympathetic outflow and impaired insulin control via changes in vagal and sympathetic balance. With advancing age, the sympathetic nervous system exhibits functional declines despite overall increased activity. Norepinephrine spillover from cardiac rises during stress—up to 2–3 times higher in older adults (60–75 years) compared to younger ones (20–30 years)—due to reduced neuronal , with transcardiac extraction dropping from 82% to 70% at rest. However, postsynaptic receptor sensitivity diminishes, blunting responses despite elevated levels, contributing to impaired stress adaptability by late adulthood. Adrenal medullary adrenaline secretion decreases by about 40% in older men, further altering sympathoadrenal balance. These changes underscore the system's lifelong plasticity but highlight vulnerabilities in maintaining during aging.

Clinical aspects

Associated disorders

Dysfunction of the sympathetic nervous system (SNS) can manifest as either underactivity or overactivity, leading to a range of clinical disorders characterized by impaired autonomic regulation. In cases of SNS underactivity, such as neurogenic (), there is a failure of sympathetic in response to postural changes, resulting in a sustained drop in systolic of more than 20 mmHg or diastolic blood pressure of more than 10 mmHg within three minutes of standing. This condition often arises from impaired central neural pathways that regulate sympathetic outflow or deficient activation of vascular adrenoceptors, leading to symptoms like , syncope, and . (), a neurodegenerative disorder, exemplifies profound SNS underactivity, where progressive loss of peripheral postganglionic sympathetic neurons causes severe , anhidrosis, and genitourinary dysfunction without central involvement. SNS overactivity, conversely, contributes to conditions involving excessive vasoconstriction or catecholamine release. Raynaud's phenomenon involves episodic vasospasm of the digits triggered by cold or stress, driven by exaggerated sympathetic reflexes and heightened sensitivity of alpha-1 and alpha-2 adrenoceptors in vascular , leading to , , and pain. , a rare catecholamine-secreting tumor of the , causes paroxysmal surges of norepinephrine and epinephrine, mimicking SNS hyperactivity and resulting in episodic , , headaches, and sweating due to overstimulation of adrenergic receptors. In spinal cord injuries at or above the T6 level, emerges as a life-threatening syndrome of uncontrolled sympathetic reflexes below the lesion, triggered by noxious stimuli like distension, causing hypertensive crises, , and severe headaches from massive imbalanced discharge. Hyperhidrosis, characterized by excessive sweating beyond physiological needs for thermoregulation, arises from overactivity of the sympathetic nervous system, which innervates eccrine sweat glands via cholinergic fibers. Primary hyperhidrosis is idiopathic and typically focal, affecting areas such as the palms, soles, axillae, and craniofacial region, often due to central dysregulation or hypersensitivity of sudomotor pathways. Secondary hyperhidrosis, in contrast, results from underlying conditions like infections, endocrine disorders, or medications that enhance sympathetic drive. This SNS-mediated disorder leads to significant psychosocial impact and is managed through various antiperspirants, medications, or surgical sympathectomy in severe cases. Chronic SNS overactivity is also implicated in psychiatric disorders such as anxiety disorders and (PTSD). In PTSD, sustained hyperactivity of the SNS, evidenced by elevated and norepinephrine levels, underlies hyperarousal symptoms including exaggerated startle responses and disturbances, reflecting a maladaptive persistence of the fight-or-flight state. Similarly, anxiety disorders feature SNS dominance with reduced parasympathetic tone, promoting persistent and elevated catecholamine release that exacerbate worry, panic, and somatic symptoms like . Recent post-2020 research highlights SNS dysregulation in long COVID, where SARS-CoV-2 infection induces autonomic imbalance, often manifesting as sympathetic overactivity or storm-like responses alongside parasympathetic inhibition. This leads to symptoms such as orthostatic intolerance, tachycardia, and fatigue, potentially due to oxidative stress and inflammatory damage to autonomic pathways, with evidence of persistent dysfunction up to 3.5 years post-infection in a significant proportion of patients. As of 2025, ongoing clinical trials, such as those under the NIH RECOVER Initiative, are evaluating treatments for autonomic nervous system dysfunction in long COVID, including interventions for tachycardia and fatigue.

Therapeutic interventions

Therapeutic interventions targeting the sympathetic nervous system primarily involve pharmacological agents that either enhance (sympathomimetics) or inhibit (sympatholytics) its activity, alongside procedural and emerging approaches to modulate sympathetic overdrive in specific conditions. These treatments leverage the system's subtypes—alpha-1, alpha-2, beta-1, and beta-2—for selective effects, minimizing off-target impacts while addressing disorders like , , , and syndromes. Receptor selectivity is crucial; for instance, beta-1 selective agents primarily affect cardiac function, whereas non-selective ones influence both cardiac and vascular or bronchial responses. Sympathomimetics activate adrenergic receptors to replicate endogenous catecholamine effects. Epinephrine, a non-selective alpha and beta , serves as the first-line intramuscular treatment for , counteracting life-threatening via alpha-1 mediated and via beta-2 mediated relaxation, with onset within minutes. Albuterol, a short-acting selective beta-2 , is administered via for acute exacerbations, promoting bronchodilation by stimulating beta-2 receptors on airway and reducing inflammatory mediator release, typically providing relief within 5-15 minutes. These agents carry risks of and arrhythmias due to beta-1 stimulation, particularly with non-selective compounds like epinephrine. Sympatholytics block adrenergic receptors to attenuate sympathetic tone. Beta-blockers, such as (non-selective, blocking beta-1 and beta-2 receptors), are widely used for , reducing by decreasing and through beta-1 antagonism, with typical dosing starting at 40-80 mg daily. Cardioselective beta-1 blockers like metoprolol offer similar antihypertensive benefits with less bronchoconstriction risk but can still cause as a common , especially in elderly patients or those with conduction abnormalities, by slowing firing. Alpha-1 selective blockers like treat via postsynaptic alpha-1 receptor antagonism, leading to and reduction, while also addressing PTSD-related nightmares by dampening noradrenergic hyperactivity in the and , with evidence from randomized trials showing reduced nightmare frequency at doses of 2-10 mg nightly. may induce as a due to rapid . Surgical interventions disrupt sympathetic pathways directly. Sympathectomy, often performed endoscopically via thoracic approaches, treats severe primary by severing the sympathetic chain at T2-T4 levels, achieving over 90% initial success in reducing palmar sweating, though compensatory occurs in up to 80% of cases postoperatively. For angina pectoris unresponsive to medical , cervical or thoracic sympathectomy reduces sympathetic cardiac innervation, decreasing myocardial oxygen demand and episodes, as demonstrated in small cohort studies with sustained benefits in select patients. These procedures risk Horner syndrome from incomplete nerve sparing. Emerging therapies focus on and targeted inhibition of sympathetic overactivity in . type A injections inhibit release at sympathetic endings, reducing overflow in (CRPS), a condition involving sympathetic dysregulation, with randomized trials showing pain reduction lasting 3-6 months post-injection into affected limbs. stimulators deliver electrical impulses to the dorsal columns, modulating sympathetic afferent signals and alleviating intractable visceral or linked to sympathetic hyperactivity, such as in CRPS or , with implantation success rates exceeding 60% in reducing use. These approaches may cause transient or device-related infections. In catecholamine crises, such as those from , guidelines emphasize preoperative alpha-blockade with non-selective agents like (10-20 mg daily, titrated to control ) to prevent hypertensive surges by antagonizing alpha receptors, followed by beta-blockers only after adequate alpha-blockade to avoid unopposed alpha stimulation and paradoxical . Intravenous is recommended for acute crises in emergency settings, rapidly reversing catecholamine-induced . The 2023 European Society of Endocrinology guidelines underscore biochemical confirmation and multidisciplinary management to mitigate risks like from excess catecholamines.

History

Early discoveries

The early understanding of the sympathetic nervous system emerged from gross anatomical dissections in the 17th and 18th centuries, constrained by the absence of microscopic techniques that limited observations to visible nerve chains and ganglia without insight into cellular or functional details. Prior to these advancements, ancient theories, such as those of , attributed visceral functions to humoral influences rather than neural control, viewing the body as governed by fluid balances without recognizing distinct nerve pathways. This perspective began shifting in the with , who through dissections identified key visceral nerve structures, including what he termed "" along the paravertebral chain, laying groundwork for a neural interpretation of involuntary functions. In 1732, Jacques-Bénigne Winslow, a Danish anatomist working in , provided the first comprehensive description and naming of the "great sympathetic nerve," referring to the paired chain of ganglia extending alongside the thoracic and lumbar , which he observed connected visceral organs in a seemingly unified manner. Winslow's work, based on human and animal dissections, marked a pivotal transition from humoral to neural theories by emphasizing the anatomical continuity of these nerves in coordinating bodily "sympathies" or interconnected responses, though functional mechanisms remained speculative without experimental validation. The 19th century brought experimental clarity through animal dissections and vivisections, revealing the thoracolumbar outflow of the sympathetic system—where preganglionic fibers originate from the thoracic (T1–T12) and upper (L1–L2) spinal segments—as anatomists traced white rami communicantes linking spinal nerves to the paravertebral chain. Key physiological experiments in the 1850s further elucidated the sympathetic system's control. In 1851, sectioned the cervical in rabbits, observing immediate , facial flushing, and increased skin temperature on the affected side, demonstrating for the first time that these nerves contain vasoconstrictor fibers regulating blood vessel tone. The following year, replicated and extended these findings in animal models, confirming the sympathetic chain's vasoconstrictor role and additionally showing that its interruption led to (pupil constriction), thereby establishing the system's involvement in pupillary dilation through opposing parasympathetic influences. These discoveries shifted focus from purely anatomical views to functional neural mechanisms, though involvement remained unknown until later.

Key physiological insights

The term "sympathetic" in the context of the derives from word sympathetikos, meaning "sharing suffering" or "affected by like feelings," reflecting the observed coordinated physiological responses across organs that mimic a . This , popularized in the by anatomist Jacobus Winslow, emphasized the interconnected nature of visceral responses, distinguishing it from the parasympathetic system. In the late 19th and early 20th centuries, J.N. Langley formalized the division of the into sympathetic and parasympathetic branches based on anatomical and functional differences. In , the term "adrenergic" emerged to describe neural transmission involving adrenaline (epinephrine) and related catecholamines, first coined in reference to the effects of these substances on sympathetic targets, as noted in early pharmacological studies by . Key advancements in the began with Otto Loewi's 1921 experiments on frog hearts, which demonstrated chemical via a substance he termed "Vagusstoff," later identified as , challenging the prevailing electrical transmission hypothesis and laying the groundwork for understanding autonomic signaling. Building on this, Walter Cannon in the 1920s integrated the sympathetic system's role in emergency responses, coining the "fight-or-flight" concept in his 1929 work to describe the coordinated activation of sympathetic nerves and release of epinephrine, which mobilizes energy for survival. This was extended in 1946 when Ulf von Euler isolated norepinephrine from sympathetic nerves, establishing it as the primary postganglionic neurotransmitter and elucidating its role in and other responses, a discovery that clarified the biochemical basis of adrenergic transmission. The 1970 Nobel Prize in Physiology or Medicine, awarded to , Ulf von Euler, and , recognized their work on storage, release, and inactivation mechanisms in sympathetic terminals, particularly norepinephrine's uptake and processes, which provided foundational insights into adrenergic signaling . In the 1970s, receptor subclassification advanced with the delineation of alpha- and beta-adrenergic subtypes, initially proposed by Raymond Ahlquist in 1948 but refined through pharmacological assays showing differential responses—alpha receptors mediating and beta receptors facilitating bronchodilation and cardiac stimulation—enabling targeted therapies. By the 2010s, neuroimaging techniques like functional MRI revealed central control mechanisms, identifying hypothalamic and networks that modulate sympathetic outflow during stress, as shown in studies correlating BOLD signals with sympathetic activity. Recent 2025 developments incorporate AI modeling to simulate sympathetic networks, with algorithms predicting risks by integrating autonomic signals and cerebral , offering predictive tools for disorders like .

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