# Lecture 5: Autonomic Nervous System Physiology ## Unit 1.6: Physiology Foundations --- ## Learning Objectives By the end of this lecture, students will be able to: 1. Compare the organization of sympathetic and parasympathetic divisions 2. Identify neurotransmitters and receptors in the autonomic nervous system 3. Describe the physiological effects of sympathetic and parasympathetic activation 4. Explain the concept of autonomic tone and dual innervation 5. Describe the adrenal medulla and its role in the stress response 6. Apply autonomic pharmacology to clinical scenarios --- ## Overview of the Autonomic Nervous System The autonomic nervous system constitutes the division of the peripheral nervous system responsible for controlling involuntary functions and maintaining internal homeostasis. Operating largely below the level of consciousness, it regulates vital functions including heart rate, blood pressure, digestion, respiration, and body temperature. The term "autonomic" reflects its self-governing nature, though higher brain centers can modulate its activity. Three divisions comprise the autonomic nervous system. The sympathetic division, originating from thoracolumbar spinal segments, mediates the "fight or flight" response that prepares the body for stressful or emergency situations. The parasympathetic division, arising from cranial nerves and sacral spinal segments, promotes "rest and digest" functions that conserve energy and maintain routine body functions. The enteric nervous system, sometimes called the "second brain," operates semi-independently within the gastrointestinal tract to control motility and secretion. The autonomic nervous system differs fundamentally from the somatic nervous system in several respects. While somatic motor neurons extend directly from the central nervous system to innervate skeletal muscle via a single neuron, autonomic pathways utilize two neurons in series—a preganglionic neuron synapsing in an autonomic ganglion with a postganglionic neuron that reaches the effector organ. Somatic motor neurons always produce excitation through acetylcholine acting at nicotinic receptors, whereas autonomic neurons can produce either excitation or inhibition depending on the neurotransmitter and receptor involved. Additionally, somatic control is voluntary, while autonomic control is involuntary. Panel A: Somatic motor pathway showing single neuron from spinal cord to skeletal muscle with acetylcholine at nicotinic receptors producing excitation. Panel B: Autonomic pathway with two neurons in series synapsing at an autonomic ganglion using acetylcholine at nicotinic receptors. Panel C: Postganglionic neuron extending to smooth muscle, cardiac muscle, or glands with various neurotransmitters. Panel D: Comparison of excitatory-only somatic effects versus variable excitatory or inhibitory autonomic effects. --- ## Sympathetic Division The sympathetic division originates from the intermediolateral cell column of spinal cord segments T1 through L2, explaining its designation as the thoracolumbar outflow. Preganglionic neurons have relatively short axons that exit the spinal cord via ventral roots and enter the sympathetic chain ganglia through white rami communicantes. These preganglionic neurons may synapse at the level they enter, ascend or descend within the chain to synapse at other levels, or pass through the chain without synapsing to reach prevertebral ganglia. The ganglia of the sympathetic division fall into two categories based on location. Paravertebral (chain) ganglia form paired columns running alongside the vertebral column from the base of the skull to the coccyx. These ganglia receive preganglionic fibers and send postganglionic fibers to structures of the head, neck, thorax, and limbs. Prevertebral (collateral) ganglia lie anterior to the aorta and include the celiac ganglion (innervating foregut structures), superior mesenteric ganglion (innervating midgut structures), and inferior mesenteric ganglion (innervating hindgut and pelvic structures). Postganglionic neurons in the sympathetic division have long axons that extend from ganglia to their target organs. At most sympathetic neuroeffector junctions, the postganglionic neuron releases norepinephrine, which acts on adrenergic receptors (α and β subtypes) on the effector cells. Notable exceptions include sympathetic innervation of sweat glands, which uses acetylcholine acting on muscarinic receptors (cholinergic sympathetic fibers), and the adrenal medulla, which receives preganglionic sympathetic fibers directly without an intervening postganglionic neuron. All preganglionic neurons in both sympathetic and parasympathetic divisions release acetylcholine acting on nicotinic receptors at the ganglionic synapse. This common ganglionic neurotransmission distinguishes the ganglion as a relay station where signal modulation and integration can occur. Panel A: Sympathetic division origin from T1-L2 spinal segments with preganglionic cell bodies in the intermediolateral horn. Panel B: Paravertebral sympathetic chain ganglia with short preganglionic and long postganglionic fibers to head, neck, thorax, and limbs. Panel C: Prevertebral ganglia including celiac, superior mesenteric, and inferior mesenteric supplying abdominal and pelvic viscera. Panel D: Neurotransmitter distribution showing acetylcholine at ganglia and norepinephrine at most effectors except cholinergic sweat glands. --- ## Parasympathetic Division The parasympathetic division arises from two distinct regions, collectively termed the craniosacral outflow. Cranial parasympathetic neurons originate in nuclei of the brainstem and exit with cranial nerves III (oculomotor), VII (facial), IX (glossopharyngeal), and X (vagus). Sacral parasympathetic neurons originate from spinal segments S2-S4 and travel in pelvic splanchnic nerves to pelvic organs. The anatomical organization of the parasympathetic division differs markedly from the sympathetic. Preganglionic neurons have long axons that travel considerable distances to reach ganglia located near or within the target organs. Postganglionic neurons consequently have very short axons connecting the ganglion to the effector. This arrangement contrasts with the sympathetic pattern of short preganglionic and long postganglionic fibers. Each cranial parasympathetic pathway has specific targets. Cranial nerve III carries fibers to the ciliary ganglion, from which postganglionic neurons innervate the pupillary sphincter (causing miosis) and ciliary muscle (enabling accommodation for near vision). Cranial nerve VII carries fibers to the pterygopalatine ganglion (innervating lacrimal and nasal glands) and submandibular ganglion (innervating submandibular and sublingual salivary glands). Cranial nerve IX carries fibers to the otic ganglion, which innervates the parotid gland. Cranial nerve X, the vagus, provides the most extensive parasympathetic distribution, sending fibers to terminal ganglia in the heart, lungs, and gastrointestinal tract from the esophagus to the splenic flexure of the colon. Sacral parasympathetic fibers from S2-S4 form the pelvic splanchnic nerves, which innervate the hindgut (descending colon, sigmoid, rectum), bladder, and reproductive organs. These fibers synapse in ganglia within or very near the target organs. Both preganglionic and postganglionic neurons of the parasympathetic division are cholinergic. Preganglionic neurons release acetylcholine acting on nicotinic receptors at ganglia (as in the sympathetic division), while postganglionic neurons release acetylcholine acting on muscarinic receptors at effector organs. Panel A: Cranial parasympathetic outflow from brainstem nuclei through cranial nerves III, VII, IX, and X to ganglia near target organs. Panel B: Vagus nerve distribution providing extensive parasympathetic innervation to thoracic and abdominal organs including heart, lungs, and GI tract. Panel C: Sacral parasympathetic outflow from S2-S4 forming pelvic splanchnic nerves to bladder, reproductive organs, and hindgut. Panel D: Cholinergic transmission throughout with acetylcholine at nicotinic ganglionic and muscarinic effector receptors. --- ## Neurotransmitters and Receptors Cholinergic receptors, activated by acetylcholine, divide into two major families based on their pharmacology. Nicotinic receptors are ligand-gated ion channels that produce rapid excitatory responses. The neural subtype (Nn) found at all autonomic ganglia and in the CNS mediates fast excitatory transmission from preganglionic to postganglionic neurons. The muscle subtype (Nm) at the neuromuscular junction mediates voluntary muscle contraction. Muscarinic receptors are G-protein coupled receptors with five subtypes (M1-M5) that produce slower, more prolonged effects. M1 receptors in the CNS and gastric parietal cells produce excitatory effects. M2 receptors in the heart slow heart rate and reduce conduction velocity. M3 receptors in smooth muscle and glands cause contraction and secretion, respectively. Adrenergic receptors, activated by norepinephrine and epinephrine, also divide into families with distinct signaling mechanisms and tissue distributions. Alpha-1 receptors couple to Gq proteins, activating phospholipase C to produce IP3 and diacylglycerol, ultimately raising intracellular calcium. These receptors mediate vasoconstriction in most vascular beds, mydriasis (pupil dilation), and contraction of the bladder internal sphincter and prostate. Alpha-2 receptors couple to Gi proteins, inhibiting adenylyl cyclase and reducing cAMP. Located presynaptically on sympathetic nerve terminals, they provide negative feedback inhibition of norepinephrine release. Postsynaptically, they contribute to vasoconstriction in some vascular beds. Beta receptors couple to Gs proteins, stimulating adenylyl cyclase and increasing cAMP. Beta-1 receptors predominate in the heart, where they increase heart rate (chronotropy), contractility (inotropy), and conduction velocity (dromotropy). Beta-2 receptors predominate in smooth muscle of the bronchi (causing relaxation and bronchodilation), blood vessels of skeletal muscle (causing vasodilation), and uterus (causing relaxation). Beta-3 receptors in adipose tissue stimulate lipolysis. The relative affinity of catecholamines for receptor subtypes has clinical significance. Norepinephrine has relatively equal affinity for alpha and beta-1 receptors but low affinity for beta-2 receptors. Epinephrine has high affinity for all receptor subtypes. These differences explain why norepinephrine predominantly causes vasoconstriction (alpha effect) while epinephrine at low doses can cause vasodilation in skeletal muscle (beta-2 effect). Panel A: Cholinergic nicotinic receptors at autonomic ganglia and neuromuscular junction functioning as ligand-gated ion channels. Panel B: Cholinergic muscarinic receptor subtypes M1, M2, and M3 with their G-protein coupling and tissue effects. Panel C: Adrenergic alpha receptor subtypes including alpha-1 causing vasoconstriction and alpha-2 providing presynaptic inhibition. Panel D: Adrenergic beta receptor subtypes with beta-1 cardiac effects, beta-2 bronchodilation and vasodilation, and beta-3 lipolysis. --- ## Organ System Effects The cardiovascular system demonstrates the complementary and often antagonistic effects of sympathetic and parasympathetic divisions. Sympathetic activation through beta-1 receptors increases heart rate, contractility, and conduction velocity, while alpha-1 activation causes vasoconstriction in most vascular beds. Parasympathetic activation through M2 receptors slows heart rate, reduces atrial contractility, and slows conduction through the AV node. Most blood vessels lack significant parasympathetic innervation, with vascular tone controlled primarily by sympathetic activity. In the respiratory system, sympathetic beta-2 receptor activation relaxes bronchial smooth muscle, producing bronchodilation and facilitating airflow during stress or exertion. Sympathetic activation also reduces bronchial secretions. Parasympathetic M3 receptor activation contracts bronchial smooth muscle, causing bronchoconstriction, and increases secretions. These opposing effects explain why beta-agonists treat asthma while parasympathetic activation can trigger asthmatic bronchospasm. Gastrointestinal function is predominantly under parasympathetic control during the "rest and digest" state. Parasympathetic activation increases motility and secretions throughout the GI tract while relaxing sphincters to facilitate movement of contents. Sympathetic activation produces opposite effects: decreased motility, decreased secretions, and sphincter contraction, inhibiting digestive activity during stress. The eye demonstrates dual innervation with clearly opposite effects. Sympathetic alpha-1 activation contracts the radial muscle of the iris, causing mydriasis (pupil dilation) and facilitating distant vision by relaxing the ciliary muscle. Parasympathetic M3 activation contracts the pupillary sphincter, causing miosis (pupil constriction) and contracts the ciliary muscle, enabling accommodation for near vision. Genitourinary function involves coordinated sympathetic and parasympathetic effects. Bladder filling requires sympathetic beta-2 activation to relax the detrusor muscle and alpha-1 activation to contract the internal sphincter. Micturition requires parasympathetic M3 activation to contract the detrusor and relax the internal sphincter. Sexual function involves parasympathetic control of erection ("point") and sympathetic control of ejaculation ("shoot"). Metabolic effects of sympathetic activation prepare the body for increased energy expenditure. Glycogenolysis in liver and muscle releases glucose. Gluconeogenesis increases hepatic glucose production. Lipolysis mobilizes fatty acids from adipose tissue. Insulin secretion is inhibited through alpha-2 receptors while glucagon secretion is stimulated, further elevating blood glucose. Panel A: Cardiovascular effects showing sympathetic beta-1 increasing heart rate and force versus parasympathetic M2 decreasing rate, with vascular alpha-1 vasoconstriction. Panel B: Respiratory and gastrointestinal effects with sympathetic beta-2 bronchodilation versus parasympathetic M3 bronchoconstriction and opposing GI motility effects. Panel C: Eye effects showing sympathetic alpha-1 mydriasis versus parasympathetic M3 miosis and accommodation. Panel D: Genitourinary effects with coordinated sympathetic and parasympathetic control of bladder filling and emptying. --- ## Autonomic Tone and Dual Innervation Autonomic tone refers to the continuous baseline activity maintained by both sympathetic and parasympathetic divisions, even at rest. This tonic activity allows for bidirectional control: an organ can be stimulated by increasing activity in one division or decreasing activity in the opposing division. The relative balance of tone varies by organ system and physiological state. The heart exemplifies the importance of autonomic tone. At rest, parasympathetic tone predominates, keeping heart rate below the intrinsic pacemaker rate of approximately 100 beats per minute. Vagal blockade with atropine increases heart rate to near 100 bpm, demonstrating the restraining effect of parasympathetic tone. Sympathetic tone contributes less at rest but becomes dominant during exercise and stress. Blood vessels, in contrast, are under predominantly sympathetic tonic control. Sympathetic blockade causes vasodilation and blood pressure reduction, while parasympathetic effects on most vessels are minimal. Most organs receive dual innervation from both sympathetic and parasympathetic divisions, typically with antagonistic effects. This arrangement provides precise control through the balance of opposing influences. However, some structures receive only sympathetic innervation. Blood vessels in skin and skeletal muscle, sweat glands, piloerector muscles, and the adrenal medulla lack parasympathetic innervation. Sympathetic control of these structures operates by modulating the degree of tonic sympathetic activity—vasodilation results from decreased sympathetic tone rather than active parasympathetic vasodilation. Some effects involve cooperation rather than antagonism between divisions. Salivation requires both divisions: parasympathetic activation produces copious watery secretions while sympathetic activation adds mucous components. Sexual function involves a sequence of parasympathetic (erection) then sympathetic (ejaculation) activity. Panel A: Cardiac autonomic tone showing parasympathetic dominance at rest keeping heart rate below intrinsic pacemaker rate. Panel B: Blood vessel tone with sympathetic-only innervation where reduced sympathetic activity causes vasodilation. Panel C: Organs with dual innervation including heart, GI tract, bladder, and eye showing antagonistic control. Panel D: Structures with single sympathetic innervation including blood vessels, sweat glands, and adrenal medulla. --- ## Adrenal Medulla The adrenal medulla functions as a modified sympathetic ganglion, representing a unique neuroendocrine structure. Developmentally, chromaffin cells of the adrenal medulla derive from neural crest cells, the same embryonic tissue that gives rise to sympathetic ganglia neurons. Unlike typical postganglionic neurons, chromaffin cells lack axons and instead release their secretory products directly into the bloodstream as hormones. The adrenal medulla receives preganglionic sympathetic innervation from the greater splanchnic nerve. When activated, these preganglionic neurons release acetylcholine that binds nicotinic receptors on chromaffin cells, triggering catecholamine release. This arrangement means that catecholamine release from the adrenal medulla requires only single-synapse transmission, enabling rapid hormonal response during stress. Chromaffin cells synthesize and release a mixture of catecholamines, with epinephrine comprising approximately 80% and norepinephrine approximately 20% of total secretion. This ratio reflects the expression of phenylethanolamine N-methyltransferase (PNMT), the enzyme that converts norepinephrine to epinephrine, which is induced by cortisol from the adjacent adrenal cortex. Epinephrine released from the adrenal medulla has widespread effects that complement and amplify the direct effects of sympathetic neural activation. Because epinephrine has high affinity for beta-2 receptors (unlike norepinephrine), adrenal medullary activation produces bronchodilation and vasodilation in skeletal muscle that would not occur with sympathetic nerve stimulation alone. At higher concentrations, epinephrine's alpha-1 effects predominate, causing vasoconstriction. The metabolic effects of epinephrine—glycogenolysis, gluconeogenesis, lipolysis—mobilize energy substrates throughout the body. The hormonal actions of adrenal catecholamines persist longer than direct sympathetic neural effects because hormones must be cleared from the blood rather than simply terminating release. This extended duration amplifies and prolongs the "fight or flight" response, providing sustained support for physical exertion or emergency situations. Panel A: Adrenal gland cross-section showing cortical zones surrounding the medulla with chromaffin cells. Panel B: Preganglionic sympathetic innervation via splanchnic nerve releasing acetylcholine onto chromaffin cell nicotinic receptors. Panel C: Catecholamine release with epinephrine comprising 80% and norepinephrine 20% entering the bloodstream. Panel D: Target organ effects of adrenal catecholamines on heart, blood vessels, lungs, liver, and adipose tissue amplifying the stress response. --- ## Autonomic Reflexes The baroreceptor reflex exemplifies rapid autonomic homeostatic regulation, maintaining blood pressure within narrow limits moment to moment. Baroreceptors in the carotid sinus and aortic arch detect arterial wall stretch that increases with rising blood pressure. When blood pressure increases, increased baroreceptor firing signals the cardiovascular center in the medulla to increase parasympathetic and decrease sympathetic output. The resulting decrease in heart rate and vasodilation returns blood pressure toward normal. Conversely, falling blood pressure reduces baroreceptor firing, triggering increased sympathetic and decreased parasympathetic activity to raise heart rate and cause vasoconstriction. This reflex operates continuously, buffering the moment-to-moment fluctuations in blood pressure that occur with posture changes and other activities. The micturition reflex coordinates bladder function through autonomic and somatic components. Bladder filling activates stretch receptors that signal spinal cord centers. When the bladder reaches threshold volume, parasympathetic activation contracts the detrusor muscle while relaxing the internal sphincter. Simultaneously, somatic motor inhibition relaxes the external sphincter. Voluntary control involves somatic motor neurons that can maintain external sphincter contraction to delay voiding or relax to permit voiding at appropriate times. The pupillary light reflex demonstrates a cranial nerve-mediated parasympathetic response. Light striking the retina activates photoreceptors, with signals traveling via the optic nerve to the pretectal nucleus. From there, bilateral connections to the Edinger-Westphal nuclei activate parasympathetic fibers traveling with cranial nerve III to the ciliary ganglion. Postganglionic parasympathetic fibers innervate the pupillary sphincter, causing bilateral pupil constriction. This reflex protects the retina from excessive light and is routinely tested as part of the neurological examination. The defecation reflex parallels the micturition reflex in organization. Rectal distension activates stretch receptors that trigger parasympathetic activation of rectal contraction and internal sphincter relaxation. As with micturition, voluntary control of the external sphincter via somatic motor neurons allows socially appropriate timing of defecation. Panel A: Baroreceptor reflex pathway from carotid sinus and aortic arch sensors through medullary cardiovascular center to sympathetic and parasympathetic effectors. Panel B: Micturition reflex with bladder stretch receptors, spinal cord center, and coordinated parasympathetic and somatic sphincter control. Panel C: Pupillary light reflex from retina through pretectal nucleus to bilateral Edinger-Westphal nuclei causing pupillary constriction. Panel D: Defecation reflex organization paralleling micturition with rectal stretch receptors and coordinated sphincter control. --- ## Autonomic Pharmacology Cholinergic drugs target various components of acetylcholine signaling and have diverse clinical applications. Direct muscarinic agonists such as pilocarpine and bethanechol mimic acetylcholine at muscarinic receptors, used respectively for glaucoma treatment (pupillary constriction reduces intraocular pressure) and urinary retention (bladder contraction). Indirect cholinergic agonists such as neostigmine and donepezil inhibit acetylcholinesterase, prolonging acetylcholine action; neostigmine treats myasthenia gravis while donepezil slows cognitive decline in Alzheimer's disease. Muscarinic antagonists such as atropine block parasympathetic effects, used for bradycardia treatment (blocks vagal slowing) and as premedication for anesthesia (reduces secretions). Ipratropium, a muscarinic antagonist that poorly crosses the blood-brain barrier, provides bronchodilation in COPD and asthma. Adrenergic drugs act on sympathetic effector organs through various receptor mechanisms. Alpha-1 agonists such as phenylephrine cause vasoconstriction, used as nasal decongestants and to raise blood pressure. Alpha-2 agonists such as clonidine reduce central sympathetic outflow and are used for hypertension treatment. Beta-1 selective agonists such as dobutamine increase cardiac contractility for heart failure treatment. Beta-2 selective agonists such as albuterol provide bronchodilation for asthma and COPD. Non-selective beta agonists such as isoproterenol activate both beta-1 and beta-2 receptors. Adrenergic antagonists block sympathetic effects. Alpha blockers such as prazosin (α1-selective) cause vasodilation for hypertension treatment and improve urinary symptoms in benign prostatic hyperplasia. Non-selective alpha blockers like phentolamine are used to manage hypertensive crises in pheochromocytoma. Beta blockers such as propranolol (non-selective) and metoprolol (β1-selective) reduce heart rate and blood pressure, used for hypertension, angina, arrhythmias, and heart failure. Panel A: Cholinergic agonists including direct muscarinic agonists and indirect acetylcholinesterase inhibitors with their clinical applications. Panel B: Cholinergic antagonists including muscarinic blockers like atropine and ipratropium for bradycardia and bronchospasm. Panel C: Adrenergic agonists organized by receptor selectivity including alpha and beta subtypes with clinical uses. Panel D: Adrenergic antagonists including alpha blockers for hypertension and beta blockers for cardiac conditions. --- ## Clinical Applications Orthostatic hypotension occurs when blood pressure fails to increase appropriately upon standing, resulting from inadequate sympathetic vasoconstriction. Normally, standing reduces venous return and activates baroreceptor reflexes that increase sympathetic tone and heart rate. Autonomic neuropathy from diabetes, Parkinson's disease, or primary autonomic failure impairs this compensatory vasoconstriction. Medications including alpha blockers, diuretics, and antidepressants can also cause or exacerbate orthostatic hypotension. Patients experience lightheadedness, visual disturbance, or syncope upon standing. Horner syndrome results from disruption of the sympathetic pathway to the face and eye at any point from the hypothalamus through the superior cervical ganglion to the eye. The classic triad includes ptosis (drooping of the upper eyelid from loss of sympathetic innervation to Müller's muscle), miosis (small pupil from unopposed parasympathetic tone), and anhidrosis (absent sweating on the affected side of the face). Causes include stroke, spinal cord lesions, Pancoast tumor compressing the sympathetic chain, and carotid artery dissection. Autonomic dysreflexia is a potentially life-threatening syndrome occurring in patients with spinal cord injuries above T6. Noxious stimuli below the level of injury (commonly bladder distension or fecal impaction) trigger massive sympathetic discharge in the isolated spinal cord below the lesion. The resulting hypertension activates baroreceptors, which signal the brainstem to increase parasympathetic output and decrease sympathetic output. However, the descending sympathetic inhibition cannot reach the spinal cord below the injury, so vasoconstriction persists while reflex bradycardia develops. Treatment requires identifying and removing the triggering stimulus. Pheochromocytoma is a catecholamine-secreting tumor of chromaffin cells, typically located in the adrenal medulla. Episodic release of epinephrine and norepinephrine causes paroxysmal hypertension, headache, sweating, and palpitations. Sustained hypertension may also occur. Diagnosis involves measuring plasma or urinary catecholamines and metabolites. Treatment requires alpha blockade (phenoxybenzamine) before beta blockade to prevent unopposed alpha-mediated vasoconstriction, followed by surgical resection. Diabetic autonomic neuropathy represents diffuse autonomic nerve damage from chronic hyperglycemia. Manifestations include gastroparesis (delayed gastric emptying causing nausea, vomiting, and glucose variability), orthostatic hypotension, neurogenic bladder (urinary retention, incontinence), erectile dysfunction, and impaired awareness of hypoglycemia (from loss of sympathetic warning symptoms). Cardiovascular autonomic neuropathy increases the risk of sudden cardiac death. Panel A: Horner syndrome showing sympathetic pathway disruption causing ptosis, miosis, and anhidrosis on the affected side. Panel B: Autonomic dysreflexia in spinal cord injury above T6 with massive sympathetic discharge and reflex bradycardia. Panel C: Pheochromocytoma catecholamine-secreting tumor causing episodic hypertension with alpha-blocker-first treatment approach. Panel D: Diabetic autonomic neuropathy affecting cardiovascular, gastrointestinal, genitourinary, and metabolic functions. --- ## Summary The autonomic nervous system controls involuntary functions through two main divisions. The sympathetic division originates from T1-L2 spinal segments and features short preganglionic neurons synapsing in paravertebral or prevertebral ganglia with long postganglionic neurons that release norepinephrine at most effectors. The parasympathetic division originates from cranial nerves and S2-S4 spinal segments with long preganglionic neurons synapsing in ganglia near target organs with short postganglionic neurons that release acetylcholine at all effectors. Cholinergic receptors include nicotinic types at ganglia and muscarinic types at parasympathetic effectors. Adrenergic receptors include alpha-1 (Gq, vasoconstriction), alpha-2 (Gi, presynaptic inhibition), and beta types (Gs, increased heart rate and contractility, bronchodilation). Autonomic tone provides continuous baseline activity allowing bidirectional control. Most organs receive dual innervation with antagonistic effects. The adrenal medulla functions as a modified sympathetic ganglion, releasing epinephrine (80%) and norepinephrine (20%) into the bloodstream to amplify and prolong the fight-or-flight response. Autonomic reflexes including the baroreceptor reflex, micturition reflex, and pupillary light reflex maintain homeostasis through rapid, coordinated responses. Autonomic drugs have widespread clinical applications: cholinergic agents for glaucoma, urinary retention, and myasthenia gravis; anticholinergics for bradycardia and bronchospasm; adrenergic agonists for asthma and hypotension; and adrenergic blockers for hypertension and heart disease. Clinical disorders of autonomic function include orthostatic hypotension, Horner syndrome, autonomic dysreflexia, and pheochromocytoma. --- ## Key Terms | Term | Definition | |------|------------| | Autonomic tone | Continuous baseline activity in both sympathetic and parasympathetic divisions enabling bidirectional control | | Dual innervation | Most organs receive input from both autonomic divisions, typically with antagonistic effects | | Adrenergic | Using norepinephrine or epinephrine as neurotransmitter, acting at α and β receptors | | Cholinergic | Using acetylcholine as neurotransmitter, acting at nicotinic or muscarinic receptors | | Chromaffin cells | Modified neural crest cells in adrenal medulla that release catecholamines into blood | | Baroreceptor reflex | Rapid autonomic reflex that buffers blood pressure changes through reciprocal sympathetic and parasympathetic adjustments | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*