Physiology 5th Ed.


The autonomic nervous system has two major divisions: the sympathetic and the parasympathetic, which often complement each other in the regulation of organ system function. A third division of the autonomic nervous system, the enteric nervous system, is located in plexuses of the gastrointestinal tract. (The enteric nervous system is discussed in Chapter 8.)

The organization of the autonomic nervous system is described in Figure 2-1 and its companion, Table 2-1. The sympathetic and parasympathetic divisions are included and, for comparison, so is the somatic nervous system.


Figure 2–1 Organization of the autonomic nervous system. The somatic nervous system is included for comparison. ACh, Acetylcholine; M, muscarinic receptor; N, nicotinic receptor; NE, norepinephrine. *Sweat glands have sympathetic cholinergic innervation.

Table 2–1 Organization of the Autonomic Nervous System


ACh, Acetylcholine; CN, cranial nerve.

*Somatic nervous system is included for comparison.


The terms sympathetic and parasympathetic are strictly anatomic terms and refer to the anatomic origin of the preganglionic neurons in the CNS (see Table 2-1). Preganglionic neurons in the sympathetic division originate in the thoracolumbar spinal cord. Preganglionic neurons in the parasympathetic division originate in the brain stem and sacral spinal cord.

The terms adrenergic and cholinergic are used to describe neurons of either division, according to which neurotransmitter they synthesize and release. Adrenergic neurons release norepinephrine; receptors for norepinephrine on the effector organs are called adrenoreceptors. Adrenoreceptors may be activated by norepinephrine, which is released from adrenergic neurons, or by epinephrine, which is secreted into the circulation by the adrenal medulla. Cholinergic neurons release ACh; receptors for ACh are called cholinoreceptors. (A third term is nonadrenergic, noncholinergic, which describes somepostganglionic parasympathetic neurons of the gastrointestinal tract that release peptides [e.g., substance P] or other substances [e.g., nitric oxide] as their neurotransmitter rather than ACh.)

To summarize, whether located in the sympathetic division or in the parasympathetic division, all preganglionic neurons release ACh and, therefore, are called cholinergic. Postganglionic neurons may be either adrenergic (they release norepinephrine) or cholinergic (they release ACh). Most postganglionic parasympathetic neurons are cholinergic; postganglionic sympathetic neurons may be either adrenergic or cholinergic.

Neuroeffector Junctions of the Autonomic Nervous System

The junctions between postganglionic autonomic neurons and their effectors (target tissues), the neuroeffector junctions, are analogous to the neuromuscular junctions of the somatic nervous system. There are, however, several structural and functional differences with the neuromuscular junction. (1) The neuromuscular junction (discussed in Chapter 1) has a discrete arrangement, whereby the “effector,” a skeletal muscle fiber, is innervated by a single motoneuron. In contrast, in the autonomic nervous system, the postganglionic neurons that innervate target tissues form diffuse, branching networks. Beads, or varicosities, line these branches and are the sites of neurotransmitter synthesis, storage, and release. The varicosities are therefore analogous to the presynaptic nerve terminals of the neuromuscular junction. (2) There is overlap in the branching networks from different postganglionic neurons, such that target tissues may be innervated by many postganglionic neurons. (3) In the autonomic nervous system, postsynaptic receptors are widely distributed on the target tissues, and there is no specialized region of receptors analogous to the motor end plate of skeletal muscle.

Sympathetic Nervous System

The overall function of the sympathetic nervous system is to mobilize the body for activity. In the extreme, if a person is exposed to a stressful situation, the sympathetic nervous system is activated with a response known as “fight or flight,” which includes increased arterial pressure, increased blood flow to active muscles, increased metabolic rate, increased blood glucose concentration, and increased mental activity and alertness. Although this response, per se, is rarely employed, the sympathetic nervous system operates continuously to modulate the functions of many organ systems such as heart, blood vessels, gastrointestinal tract, bronchi, and sweat glands.

Figure 2-2 depicts the organization of the sympathetic nervous system in relation to the spinal cord, the sympathetic ganglia, and the effector organs in the periphery. The preganglionic sympathetic neurons originate in nuclei of the thoracolumbar spinal cord, leave the spinal cord via the ventral motor roots and white rami, and project either to the paravertebral ganglia of the sympathetic chain or to a series of prevertebral ganglia. Thus, one category of preganglionic neuron synapses on postganglionic neurons within the sympathetic chain. These synapses may occur in ganglia at the same segmental level of the chain, or the preganglionic fibers may turn in the cranial or caudal direction and innervate ganglia at higher or lower levels in the chain, thereby permitting synapses in multiple ganglia (consistent with the diffuseness of sympathetic functions). The other category of preganglionic neuron passes through the sympathetic chain without synapsing and continues on to synapse in prevertebral ganglia (celiac, superior mesenteric, and inferior mesenteric) that supply visceral organs, glands, and the enteric nervous system of the gastrointestinal tract. In the ganglia, the preganglionic neurons synapse on postganglionic neurons, which travel to the periphery and innervate the effector organs.


Figure 2–2 Innervation of the sympathetic nervous system. Preganglionic neurons originate in thoracic and lumbar segments of the spinal cord (T1–L3).

The features of the sympathetic nervous system discussed in the following sections are listed in Table 2-1 and are illustrated in Figure 2-2.

Origin of Preganglionic Neurons

The preganglionic neurons of the sympathetic division arise from nuclei in the thoracic and lumbar spinal cord segments, specifically from the first thoracic segment to the third lumbar segment (T1–L3). Thus, the sympathetic division is referred to as thoracolumbar.

Generally, the origin of preganglionic neurons in the spinal cord is anatomically consistent with the projection to the periphery. Thus, the sympathetic pathways to organs in the thorax (e.g., heart) have preganglionic neurons originating in the upper thoracic spinal cord. Sympathetic pathways to organs in the pelvis (e.g., colon, genitals) have preganglionic neurons that originate in the lumbar spinal cord. Blood vessels, thermoregulatory sweat glands, and pilomotor muscles of the skin have preganglionic neurons that synapse on multiple postganglionic neurons up and down the sympathetic chain, reflecting their broad distribution throughout the body.

Location of Autonomic Ganglia

The ganglia of the sympathetic nervous system are located near the spinal cord, either in the paravertebral ganglia (known as the sympathetic chain) or in the prevertebral ganglia. Again, the anatomy is logical. The superior cervical ganglion projects to organs in the head such as the eyes and the salivary glands. The celiac ganglion projects to the stomach and the small intestine. The superior mesenteric ganglion projects to the small and large intestine, and the inferior mesenteric ganglion projects to the lower large intestine, anus, bladder, and genitalia.

The adrenal medulla is simply a specialized sympathetic ganglion whose preganglionic neurons originate in the thoracic spinal cord (T5–T9), pass through the sympathetic chain and the celiac ganglion without synapsing, and travel in the greater splanchnic nerve to the adrenal gland.

Length of Preganglionic and Postganglionic Axons

Because the sympathetic ganglia are located near the spinal cord, the preganglionic nerve axons are short and the postganglionic nerve axons are long (so that they can reach the peripheral effector organs).

Neurotransmitters and Types of Receptors

Preganglionic neurons of the sympathetic division are always cholinergic. They release ACh, which interacts with nicotinic receptors on the cell bodies of postganglionic neurons. Postganglionic neuronsof the sympathetic division are adrenergic in all of the effector organs, except in the thermoregulatory sweat glands (where they are cholinergic). The effector organs that are innervated by sympathetic adrenergic neurons have one or more of the following types of adrenoreceptors: alpha1, alpha2, beta1, or beta2 (α1, α2, β1, or β2). The thermoregulatory sweat glands innervated by sympathetic cholinergic neurons have muscarinic cholinoreceptors.

Sympathetic Adrenergic Varicosities

As described previously, sympathetic postganglionic adrenergic nerves release their neurotransmitters from varicosities onto their target tissues (e.g., vascular smooth muscle). The sympathetic adrenergic varicosities contain both the classic neurotransmitter (norepinephrine) and nonclassic neurotransmitters (ATP and neuropeptide Y). The classic neurotransmitter, norepinephrine, is synthesized from tyrosine in the varicosities (see Fig. 1-18) and stored in small dense-core vesicles, ready for release; these small dense-core vesicles also contain dopamine β-hydroxylase, which catalyzes the conversion of dopamine to norepinephrine (the final step in the synthetic pathway), and ATP.ATP is said to be “colocalized” with norepinephrine. A separate group of large dense-core vesicles contain neuropeptide Y.

When sympathetic postganglionic adrenergic neurons are stimulated, norepinephrine and ATP are released from the small dense-core vesicles. Both norepinephrine and ATP serve as neurotransmitters at the neuroeffector junction, binding to and activating their respective receptors on the target tissue (e.g., vascular smooth muscle). Actually, ATP acts first, binding to purinergic receptors on the target tissue and causing a physiologic effect (e.g., contraction of the vascular smooth muscle). The action of norepinephrine follows ATP; norepinephrine binds to its receptors on the target tissue (e.g., α1-adrenergic receptors on vascular smooth muscle) and causes a second, more prolonged contraction. Finally, with more intense or higher-frequency stimulation, the large dense-core vesicles release neuropeptide Y, which binds to its receptor on the target tissue, causing a third, slower phase of contraction.

Adrenal Medulla

The adrenal medulla is a specialized ganglion in the sympathetic division of the autonomic nervous system. The cell bodies of its preganglionic neurons are located in the thoracic spinal cord. The axons of these preganglionic neurons travel in the greater splanchnic nerve to the adrenal medulla, where they synapse on chromaffin cells and release ACh, which activates nicotinic receptors. When activated, the chromaffin cells of the adrenal medulla secrete catecholamines (epinephrine and norepinephrine) into the general circulation. In contrast with sympathetic postganglionic neurons, which release only norepinephrine, the adrenal medulla secretes mainly epinephrine (80%) and a small amount of norepinephrine (20%). The reason for this difference is the presence of phenylethanolamine-N-methyltransferase (PNMT) in the adrenal medulla, but not in sympathetic postganglionic adrenergic neurons (see Fig. 1-18). PNMT catalyzes the conversion of norepinephrine to epinephrine, a step that, interestingly, requires cortisol from the nearby adrenal cortex; cortisol is supplied to the adrenal medulla in venous effluent from the adrenal cortex.

A tumor of the adrenal medulla, or pheochromocytoma, may be located on or near the adrenal medulla, or at a distant (ectopic) location in the body (Box 2-1). Unlike the normal adrenal medulla, which secretes mainly epinephrine, a pheochromocytoma secretes mainly norepinephrine, which is explained by the fact that the tumor is too far from the adrenal cortex to receive the cortisol that is required by PNMT.

BOX 2–1 Clinical Physiology: Pheochromocytoma

DESCRIPTION OF CASE. A 48-year-old woman visits her physician complaining of what she calls “panic attacks.” She reports that she has experienced a racing heart and that she can feel (and even see) her heart pounding in her chest. She also complains of throbbing headaches, cold hands and cold feet, feeling hot, visual disturbances, and nausea and vomiting. In the physician’s office, her blood pressure is severely elevated (230/125). She is admitted to the hospital for evaluation of her hypertension.

A 24-hour urine sample reveals elevated levels of metanephrine, normetanephrine, and 3-methoxy-4-hydroxymandelic acid (VMA). After the physician rules out other causes for hypertension, he concludes that she has a tumor of the adrenal medulla, called a pheochromocytoma. A computerized tomographic scan of the abdomen reveals a 3.5-cm mass on her right adrenal medulla. The patient is administered an α1 antagonist, and surgery is performed. The woman recovers fully; her blood pressure returns to normal, and her other symptoms disappear.

EXPLANATION OF CASE. The woman has a classic pheochromocytoma, a tumor of the chromaffin cells of the adrenal medulla. The tumor secretes excessive amounts of norepinephrine and epinephrine, which produce all of the woman’s symptoms and result in elevated levels of catecholamine metabolites in her urine. In contrast to normal adrenal medulla, which secretes mainly epinephrine, pheochromocytomas secrete mainly norepinephrine.

The patient’s symptoms can be interpreted by understanding the physiologic effects of catecholamines. Any tissue where adrenoreceptors are present will be activated by the increased levels of epinephrine and norepinephrine, which reach the tissues via the circulation. The woman’s most prominent symptoms are cardiovascular: pounding heart, increased heart rate, increased blood pressure, and cold hands and feet. These symptoms can be understood by considering the functions of adrenoreceptors in the heart and blood vessels. The increased amounts of circulating catecholamines activated β1 receptors in the heart, increasing the heart rate and increasing contractility (pounding of the heart). Activation of α1 receptors in vascular smooth muscle of the skin produced vasoconstriction, which presented as cold hands and feet. The patient felt hot, however, because this vasoconstriction in the skin impaired the ability to dissipate heat. Her extremely elevated blood pressure was caused by the combination of increased heart rate, increased contractility, and increased constriction (resistance) of the blood vessels. The patient’s headache was secondary to her elevated blood pressure.

The woman’s other symptoms also can be explained by the activation of adrenoreceptors in other organ systems (i.e., gastrointestinal symptoms of nausea and vomiting and visual disturbances).

TREATMENT. The patient’s treatment consisted of locating and excising the tumor, thereby removing the source of excess catecholamines. Alternatively, if the tumor had not been excised, the woman could have been treated pharmacologically with a combination of α1 antagonists (e.g., phenoxybenzamine or prazosin) and β1 antagonists (e.g., propranolol) to prevent the actions of the endogenous catecholamines at the receptor level.

Fight or Flight Response

The body responds to fear, extreme stress, and intense exercise with a massive, coordinated activation of the sympathetic nervous system including the adrenal medulla. This activation, the fight or flight response, ensures that the body can respond appropriately to a stressful situation (e.g., take a difficult exam, run away from a burning house, fight an attacker). The response includes increases in heart rate, cardiac output, and blood pressure; redistribution of blood flow away from skin, kidneys, and splanchnic regions and toward skeletal muscle; increased ventilation, with dilation of the airways; decreased gastrointestinal motility and secretions; and increased blood glucose concentration.

Parasympathetic Nervous System

The overall function of the parasympathetic nervous system is restorative, to conserve energy.Figure 2-3 depicts the organization of the parasympathetic nervous system in relation to the CNS (brain stem and spinal cord), the parasympathetic ganglia, and the effector organs. Preganglionic neurons of the parasympathetic division have their cell bodies in either the brain stem (midbrain, pons, and medulla) or the sacral spinal cord. Preganglionic axons project to a series of ganglia located near or in the effector organs.


Figure 2–3 Innervation of the parasympathetic nervous system. Preganglionic neurons originate in nuclei of the brain stem (midbrain, pons, medulla) and in sacral segments (S2–S4) of the spinal cord. CN, Cranial nerve.

The following features of the parasympathetic nervous system can be noted and compared with the sympathetic nervous system (see Table 2-1 and Fig. 2-3).

Origin of Preganglionic Neurons

Preganglionic neurons of the parasympathetic division arise from nuclei of cranial nerves (CN) III, VII, IX, and X or from sacral spinal cord segments S2–S4; therefore, the parasympathetic division is called craniosacral. As in the sympathetic division, the origin of the preganglionic neurons in the CNS is consistent with the projection to effector organs in the periphery. For example, the parasympathetic innervation of eye muscles originates in the Edinger-Westphal nucleus in the midbrain and travels to the periphery in CN III; the parasympathetic innervation of the heart, bronchioles, and gastrointestinal tract originates in nuclei of the medulla and travels to the periphery in CN X (vagus nerve); and the parasympathetic innervation of the genitourinary organs originates in the sacral spinal cord and travels to the periphery in the pelvic nerves.

Location of Autonomic Ganglia

In contrast to the sympathetic ganglia, which are located near the CNS, the ganglia of the parasympathetic nervous system are located near, on, or in the effector organs (e.g., ciliary, pterygopalatine, submandibular, otic).

Length of Preganglionic and Postganglionic Axons

The relative length of preganglionic and postganglionic axons in the parasympathetic division is the reverse of the relative lengths in the sympathetic division. This difference reflects the location of the ganglia. The parasympathetic ganglia are located near or in the effector organs; therefore, the preganglionic neurons have long axons and the postganglionic neurons have short axons.

Neurotransmitters and Types of Receptors

As in the sympathetic division, all preganglionic neurons are cholinergic and release ACh, which interacts at nicotinic receptors on the cell bodies of postganglionic neurons. Most postganglionic neuronsof the parasympathetic division are also cholinergic. Receptors for ACh in the effector organs are muscarinic receptors rather than nicotinic receptors. Thus, ACh released from preganglionic neurons of the parasympathetic division activates nicotinic receptors, whereas ACh released from postganglionic neurons of the parasympathetic division activates muscarinic receptors. These receptors and their functions are distinguished by the drugs that activate or inhibit them (Table 2-2).

Table 2–2 Prototypes of Agonists and Antagonists to Autonomic Receptors








































Curare (blocks neuromuscular N1 receptors)


Hexamethonium (blocks ganglionic N2 receptors)







ACh, Acetylcholine.

Parasympathetic Cholinergic Varicosities

As described previously, parasympathetic postganglionic cholinergic nerves release their neurotransmitters from varicosities onto their target tissues (e.g., smooth muscle). The parasympathetic cholinergic varicosities release both the classic neurotransmitter (ACh) and nonclassic neurotransmitters (e.g., vasoactive intestinal peptide [VIP], nitric oxide [NO]). The classic neurotransmitter, ACh, is synthesized in the varicosities from choline and acetyl CoA (see Fig. 1-17) and stored in small, clear vesicles. A separate group of large dense-core vesicles contains peptides such as VIP. Lastly, the varicosities contain nitric oxide synthase and can synthesize NO on demand.

When parasympathetic postganglionic cholinergic neurons are stimulated, ACh is released from the varicosities and binds to muscarinic receptors on the target tissue, which direct its physiologic action. With intense or high-frequency stimulation, the large dense-core vesicles release their peptides (e.g., VIP), which bind to receptors on the target tissues and augment the actions of ACh.

Autonomic Innervation of the Organ Systems

Table 2-3 serves as a reference for information concerning autonomic control of organ system function. This table lists the sympathetic and parasympathetic innervations of the major organ systems and the receptor types that are present in these tissues. Table 2-3 will be most valuable if the information it contains is seen as a set of recurring themes rather than as a random list of actions and receptors.

Table 2–3 Effects of the Autonomic Nervous System on Organ System Function


AV, Atrioventricular; EDRF, endothelial-derived relaxing factor; M, muscarinic receptor; SA, sinoatrial.

*Sympathetic cholinergic neurons.

Reciprocal Functions—Sympathetic and Parasympathetic

Most organs have both sympathetic and parasympathetic innervation. These innervations operate reciprocally or synergistically to produce coordinated responses. For example, the heart has both sympathetic and parasympathetic innervations that function reciprocally to regulate heart rate, conduction velocity, and the force of contraction (contractility). The smooth muscle walls of the gastrointestinal tract and the bladder have both sympathetic innervation (which produces relaxation) and parasympathetic innervation (which produces contraction). The radial muscles of the iris are responsible for dilation of the pupil (mydriasis) and have sympathetic innervation; the circular muscle of the iris is responsible for constriction of the pupil (miosis) and has parasympathetic innervation. In this example of the eye muscles, different muscles control pupil size, but the overall effects of sympathetic and parasympathetic activity are reciprocal. In the male genitalia, sympathetic activity controls ejaculation and parasympathetic activity controls erection, which, together, are responsible for the male sexual response.

The following three examples further illustrate the reciprocity and synergism of the sympathetic and parasympathetic divisions.


The autonomic innervation of the sinoatrial (SAnode in the heart is an excellent example of coordinated control of function. The SA node is the normal pacemaker of the heart, and its rate of depolarization sets the overall heart rate. The SA node has both sympathetic and parasympathetic innervations, which function reciprocally to modulate the heart rate. Thus, an increase in sympathetic activity increases heart rate, and an increase in parasympathetic activity decreases heart rate. These reciprocal functions are illustrated as follows: If there is a decrease in blood pressure, vasomotor centers in the brain stem respond to this decrease and produce, simultaneously, an increase in sympathetic activity to the SA node and a decrease in parasympathetic activity. Each of these actions, directed and coordinated by the brain stem vasomotor center, has the effect of increasing heart rate. The sympathetic and parasympathetic actions do not compete with each other but work synergistically to increase the heart rate (which helps restore normal blood pressure).


The urinary bladder is another example of reciprocal innervations by sympathetic and parasympathetic divisions (Fig. 2-4). In adults, micturition, or emptying of the bladder, is under voluntary control because the external sphincter is composed of skeletal muscle. However, the micturition reflex itself is controlled by the autonomic nervous system. This reflex occurs when the bladder is sensed as being “full.” The detrusor muscle of the bladder wall and the internal bladder sphincter are composed of smooth muscle; each has both sympathetic and parasympathetic innervations. The sympathetic innervation of the detrusor muscle and the internal sphincter originates in the lumbar spinal cord (L1–L3), and the parasympathetic innervation originates in the sacral spinal cord (S2–S4).


Figure 2–4 Autonomic control of bladder function. During filling of the bladder, sympathetic control predominates, causing relaxation of the detrusor muscle and contraction of the internal sphincter. During micturition, parasympathetic control predominates, causing contraction of the detrusor muscle and relaxation of the internal sphincter. Dashed lines represent sympathetic innervation; solid lines represent parasympathetic innervation. α1, Adrenoreceptor in internal sphincter; β2, adrenoreceptor in detrusor muscle; L1–L3, lumbar segments; M, muscarinic cholinoreceptor in detrusor muscle and internal sphincter; S2–S4, sacral segments.

When the bladder is filling with urine, sympathetic control predominates. This sympathetic activity produces relaxation of the detrusor muscle, via β2 receptors, and contraction of the internal sphincter muscle, via α1 receptors. The external sphincter is simultaneously closed by trained voluntary action. When the muscle wall is relaxed and the sphincters are closed, the bladder can fill with urine.

When the bladder is full, this fullness is sensed by mechanoreceptors in the bladder wall, and afferent neurons transmit this information to the spinal cord and then to the brain stem. The micturition reflex is coordinated by centers in the midbrain, and now parasympathetic control predominates. Parasympathetic activity produces contraction of the detrusor muscle (to increase pressure and eject urine) and relaxation of the internal sphincters. Simultaneously, the external sphincter is relaxed by a voluntary action.

Clearly, the sympathetic and parasympathetic actions on the bladder structures are opposite, but coordinated: The sympathetic actions dominate for bladder filling, and the parasympathetic actions dominate for bladder emptying.


The size of the pupil is reciprocally controlled by two muscles of the iris: the pupillary dilator (radial) muscle and pupillary constrictor (sphincter) muscle. The pupillary dilator muscle is controlled by sympathetic innervation through α1 receptors. Activation of these α1 receptors causes constriction of the radial muscle, which causes dilation of the pupil, or mydriasis. The pupillary constrictor muscle is controlled by parasympathetic innervation through muscarinic receptors. Activation of these muscarinic receptors causes constriction of the sphincter muscle, which causes constriction of the pupil, or miosis.

For example, in the pupillary light reflex, light strikes the retina and, through a series of CNS connections, activates parasympathetic preganglionic nerves in the Edinger-Westphal nucleus; activation of these parasympathetic fibers causes contraction of the sphincter muscle and pupillary constriction. In the accommodation response, a blurred retinal image activates parasympathetic preganglionic neurons in the Edinger-Westphal nuclei and leads to contraction of the sphincter muscle and pupillary constriction. At the same time, the ciliary muscle contracts, causing the lens to “round up” and its refractive power to increase.

There are some notable exceptions to the generalization of reciprocal innervation. Several organs have only sympathetic innervation: sweat glands, vascular smooth muscle, pilomotor muscles of the skin, liver, adipose tissue, and kidney.

Coordination of Function within Organs

Coordination of function within the organ systems, as orchestrated by the autonomic nervous system, is another recurring physiologic theme (Box 2-2).

BOX 2–2 Clinical Physiology: Horner Syndrome

DESCRIPTION OF CASE. A 66-year-old man who suffered a stroke on the right side has a drooping right eyelid (ptosis), constriction of his right pupil (miosis), and lack of sweating on the right side of his face (anhidrosis). His physician orders a test with cocaine eye drops. When a solution of 10% cocaine was applied in the left eye, it caused dilation of the pupil (mydriasis). However, when the cocaine solution was applied in the right eye, it failed to cause dilation of that pupil.

EXPLANATION OF CASE. The man has a classic case of Horner syndrome, secondary to his stroke. In this syndrome, there is loss of sympathetic innervation on the affected side of the face. Thus, the loss of sympathetic innervation to smooth muscle elevating the right eyelid caused ptosis on the right side. The loss of sympathetic innervation of the right pupillary dilator muscle caused constriction of the right pupil. And loss of sympathetic innervation of the sweat glands of the right side of the face caused anhidrosis on the right side.

When cocaine drops were instilled in the left eye (the unaffected side), the cocaine blocked reuptake of norepinephrine into sympathetic nerves innervating the pupillary dilator muscle; with higher norepinephrine levels in those adrenergic synapses, there was constriction of the radial muscle of the iris, leading to prolonged dilation of the pupil. When cocaine drops were instilled in the right eye, because there was less norepinephrine in those synapses, pupillary dilation did not occur.

TREATMENT. The treatment of Horner syndrome is to address the underlying cause.

This control is exquisitely clear, for example, when considering the function of the urinary bladder. In this organ, there must be a timely coordination between activity of the detrusor muscle in the bladder wall and in the sphincters (see Fig. 2-4). Thus, sympathetic activity dominates when the bladder is filling to produce relaxation of the bladder wall and, simultaneously, contraction of the internal bladder sphincter. The bladder can fill because the bladder wall is relaxed and the sphincter is closed. During micturition, parasympathetic activity dominates, producing contraction of the bladder wall and, simultaneously, relaxation of the sphincter.

Similar reasoning can be applied to the autonomic control of the gastrointestinal tract: Contraction of the wall of the gastrointestinal tract is accompanied by relaxation of the sphincters (parasympathetic), allowing the contents of the gastrointestinal tract to be propelled forward. Relaxation of the wall of the gastrointestinal tract is accompanied by contraction of the sphincters (sympathetic); the combined effect of these actions is to slow or stop movement of the contents.

Types of Receptors

Inspection of Table 2-3 permits some generalizations about types of receptors and their mechanisms of action. These generalizations are as follows: (1) In the parasympathetic division, effector organs have only muscarinic receptors. (2) In the sympathetic division, there are multiple receptor types in effector organs including the four adrenoreceptors (α1, α2, β1, β2), and in tissues with sympathetic cholinergic innervation, there are muscarinic receptors. (3) Among the sympathetic adrenoreceptors, receptor type is related to function. The α receptors and α1 receptors cause contraction of smooth muscle such as vascular smooth muscle, gastrointestinal and bladder sphincters, pilomotor muscles, and the radial muscle of the iris. The β1 receptors are involved in metabolic functions such as gluconeogenesis, lipolysis, renin secretion, and in all functions in the heart. The β2 receptors cause relaxation of smooth muscle in bronchioles, wall of the bladder, and wall of the gastrointestinal tract.

Hypothalamic and Brain Stem Centers

Centers in the hypothalamus and brain stem coordinate the autonomic regulation of organ system functions. Figure 2-5 summarizes the locations of these centers, which are responsible for temperature regulation, thirst, food intake (satiety), micturition, breathing, and cardiovascular (vasomotor) function. For example, the vasomotor center receives information about blood pressure from baroreceptors in the carotid sinus and compares this information to a blood pressure set point. If corrections are necessary, the vasomotor center orchestrates changes in output of both the sympathetic and the parasympathetic innervation of the heart and blood vessels to bring about the necessary change in blood pressure. These higher autonomic centers are discussed throughout this book in the context of each organ system.


Figure 2–5 Autonomic centers in the hypothalamus and brain stem. CI, First cervical spinal cord segment.