autonomic nervous system
autonomic nervous system
How do these extraordinary bodily reactions happen? You certainly have not willed your body to behave in this way. Nor, in more usual circumstances, does one will the heart to vary its rate of beating, or the gut to perform its functions, or the many other continuous internal communications and adjustments that keep the body ticking over. All of these reflect activity of the autonomic nervous system (ANS). The system has two components, sympathetic and parasympathetic, corresponding to two sets of nerve fibres streaming out from the spinal cord and brainstem, running towards all the organs they affect.
The autonomy that its name implies is a primary characteristic of the ANS: it is responsible for the body's involuntary reactions to emergencies and for most of our life-support functions except breathing. It also serves as an essential adjunct to conscious voluntary or emotional reactions. For instance, it switches on the digestive system at the time of a meal, and orchestrates the whole subsequent sequence of absorption, storage, or utilization of nutrients according to the body's changing requirements. It also makes sure that waste material is held until the voluntary go-ahead is given to defecate: if control is undeveloped (in babies) or lost (in the incontinent), there is automatic defecation. The ANS regulates the heart by speeding or slowing the beat and altering the force of its pumping. It regulates the calibre of blood vessels to vary the distribution of blood to the organs, whilst also maintaining the correct blood pressure. It adjusts the resistance to airflow in and out of the lungs by changing the diameter of the branches of the bronchial tree. It regulates body temperature by varying the blood flow to the skin and by the control of sweating. It varies the size of the pupil and the thickness of the lens of the eyes to adjust for brightness and for distance. It serves reproductive behaviour by controlling erection of the penis and ejaculation in the male, and engorgement of the nipples and clitoris in the female.
All of these apparently diverse actions and more derive from a fine balance between stimulation and inhibition of the smooth (involuntary) muscle (which forms the walls of the several types of tubes in the body), the heart muscle and its pacemaker, and the secretion of substances from glandular cells.
The ANS and its relation to the central nervous systemAnatomically, the brain and spinal cord constitute the central nervous system (CNS) and the nerve pathways outside of the skull and vertebral column are the peripheral nervous system. But, on functional grounds, the nervous system is also divided into the somatic and autonomic systems. Each of these has pathways both within the central nervous system and outside it. The somatic system has (sensory) input from muscles, joints, and body surface, and (motor) output connections to ordinary (skeletal or ‘voluntary’) muscles. It is responsible for many types of conscious bodily sensation and for the voluntary control of movement — all providing for interaction with the outside world. In contrast, the ANS by traditional definition, has only one-way, outgoing connections. (Its activity is however influenced by a great deal of sensory information, especially that coming in along so-called visceral afferent nerves from the internal organs, signalling such things as the fullness of the stomach or the pressure in the arteries.)
The peripheral nerve fibres (axons) of the ANS have their cell bodies in the brain stem and the spinal cord. These nerve cells are influenced by fibres descending within the central nervous system from higher levels, notably from the hypothalamus, which contains many of the control centres for homeostasis, the process of keeping the internal environment of the body constant.
The axons of the ANS that leave the spinal cord and brain are called ‘preganglionic’ fibres because they end in ganglia — swellings containing ‘postganglionic’ nerve cells, with which the preganglionic fibres form synaptic connections. The fibres of these postganglionic cells run out to the final destinations — in the gut, the heart, the blood vessels, and so on — where they make contact with the effector cells (smooth muscle, secretory cells, etc.)
The substance acetylcholine, first isolated and identified in the late nineteenth century, when injected has many actions on the body similar to those occurring during ANS activity. This is because acetylcholine is the natural chemical neurotransmitter released by the endings of preganglionic fibres as a result of nerve impulses (action potentials) arriving along those axons.
Sympathetic and parasympathetic subdivisions.The two components of the ANS differ in a number of ways:(i) The origin of the preganglionic nerves: sympathetic from much of the length of the spinal cord, parasympathetic from the brain stem and the lowest part of the spinal cord.(ii) The position of the ganglia: sympathetic ganglia lie close to the spinal cord; parasympathetic ganglia are buried in the final target organ. Hence sympathetic postganglionic fibres tend to be much longer than parasympathetic.(iii) The chemical transmitter produced at the terminals of the postganglionic fibres in the effector organ: mostly acetylcholine for parasympathetic and noradrenaline (norepinephrine) for sympathetic.
Sympathetic divisionSympathetic preganglionic nerve cell bodies are found in the lateral part of the grey matter of the spinal cord, throughout many segments, from the upper thoracic down to the upper lumbar level. Their axons leave (like all axons that transmit impulses out of the spinal cord) in the anterior (ventral) nerve roots that emerge from between the vertebrae. These preganglionic fibres run a short distance from the vertebral column and terminate in a chain of interconnected sympathetic ganglia, behind the pleura or the peritoneum (the membranes that respectively line the thoracic and abdominal walls). The postganglionic nerve fibres from the cells in these ganglia run out to every part of the body, except the CNS itself (although they do innervate the membranes that surround the brain and spinal cord). Sympathetic nerves run along with all arteries and veins down to their smallest branches, supplying all types of blood vessel except capillaries; from the thoracic ganglia, they supply the eyes and the heart and lungs; in the abdomen, they are distributed in the rays of the solar plexus, to be distributed to the viscera. In the pelvis, they reach the bladder and rectum, and the sphincters that control voiding.
There is one important exception to this plan. Some preganglionic fibres go directly to the medulla of the adrenal gland, whose cells originate from the same embryonic tissue as those of the sympathetic ganglia. Preganglionic fibres act on adrenal cells (through the production of acetylcholine) just as if those cells were ganglionic nerve cells. But the adrenal cells release hormones (adrenaline and noradrenaline, with a little dopamine) into the blood — a process known as neuroendocrine secretion — instead of transmitting impulses via a postganglionic nerve fibre.
The best known action of the sympathetic system (and of the adrenaline produced by the adrenal gland) is the dramatic ‘fight or flight’ reaction. The heart beats faster and more strongly. Blood vessels are constricted and flow reduced in regions, such as the gut, where blood supply is not vital, but not where ample blood supply is needed to deal with the emergency — brain, heart, and muscle. Gut movements are inhibited. Urination and defecation are postponed by relaxation of the appropriate gut muscles; the pupils are dilated and the bronchial tubes are relaxed and widened. However, the ‘fight or flight’ reaction is only an exaggeration of routine sympathetic nervous activity that is going on all the time, modulating heart rate, setting the diameter of blood vessels to redistribute the blood, and so forth. Adrenaline itself has many effects on the circulation and the metabolism, which support any sudden demand for extra energy expenditure.
Parasympathetic divisionThe parasympathetic outflow comes in two parts, from opposite ends of the CNS. The cranial component originates in the brain stem and leaves through the base of the skull in the vagus (wandering) nerves. The sacral component has its cell bodies in the lowest part of the spinal cord, with their fibres emerging through perforations in the sacrum — the terminal extension of the spinal column.
The cranial and the sacral components of the parasympathetic system between them distribute themselves around the whole of the head and the trunk. An additional cranial component, which does not leave the skull, supplies the eyes. In the thorax, the influence of the parasympathetic fibres of the vagus nerves on the heart is to slow it down; in the abdomen, their function is to activate the gut and its associated organs. The wandering vagus meets the territory of the parasympathetic outflow from the sacral spinal cord at a point in the colon. In the pelvis, the sacral component innervates the bladder and rectum, where it mediates voiding. In most of the body parasympathetic nerves have no action on blood vessels, but the brain and the penis are major exceptions: parasympathetic stimulation causes their blood vessels to relax, by release of nitric oxide as neurotransmitter.
In overwhelming circumstances, various actions of parasympathetic nerves slow the heart and lower the blood pressure, depriving the brain of its blood supply — causing fainting and thus withdrawing the conscious person from the shocking or frightening experience; stimulation of the gut causes involuntary defecation — ‘scared shitless’. In the most extreme conditions the inhibition of the heart can be so severe that it causes death: this is the probable origin of so-called Voodoo death and other forms of death without obvious cause.
Although the sympathetic and parasympathetic systems often seem to have opposite actions, for instance in their influences on the heart, they normally work in a complementary fashion, counterbalancing each other and being regulated together to produce fine control of the body's life-support functions.
Historical background: the discovery of chemical transmissionThe concept of the ANS is not new. Galen, in the second century ad, described the sympathetic chain, the rami communicans (the bundles of preganglionic fibres coming from the spinal cord), and the path of the vagus nerves. In the seventeenth century the British physician Thomas Willis produced clear descriptions of the component parts of the system; he gave the name ‘solar plexus’ to the radiating nerve fibres in the abdomen because they reminded him of the sun. Willis and his contemporaries described the ‘intercostal’ (sympathetic) and ‘wandering’ (vagus) nerves, and he demonstrated that cutting the vagus nerves caused ‘trembling’ of the heart. By the middle of the eighteenth century similar experiments had revealed that branches of the ‘intercostal’ system affected the functions of the eye, and that the ‘wandering nerve’ was associated with the control of involuntary movements of the viscera.
The word ‘autonomic’ was introduced by the Cambridge physiologist J. N. Langley in the late nineteenth century. It was the work of Langley and his colleague W. H. Gaskell that established our modern understanding of the autonomic nervous system and its integration with the CNS. Langley's observations of the effects of cutting nerves and of applying specific drugs at different points in the ANS led to the realization that there must be specialized sites of action on the cells of end-organs and ganglia, where the autonomic nerves exert their effects. From his experiments, and from the work of Paul Ehrlich in Germany, emerged one of the most powerful concepts in twentieth-century biomedical sciences, the receptor theory. Any substance in the vicinity of a cell, however it got there, usually has an action on that cell only if specific receptor molecules, into which that substance ‘fits’, are present in the cell's membrane. Thus neurotransmitters and hormones are matched to their appropriate targets, and many drugs work by mimicking these natural substances or antagonizing them by blocking the receptors.
This theory has been applied to account for cell–cell and drug–cell interactions in all manner of living tissues. It can explain not only transmission at the ganglia and at the end organs of the ANS, but almost all nerve-to-nerve and nerve-to-tissue communication in the entire nervous system, and all other cell-to-cell signalling mediated by substances released in the immediate neighbourhood, or by hormones circulating in the blood.
Gaskell's studies were predominantly anatomical, and his detailed histological descriptions of the structure and connections of the nerve fibres and ganglia contributed greatly to the unravelling of the component parts of the system, especially his identification of the two major nervous outflows, the thoracolumbar (sympathetic) and craniosacral (parasympathetic) and the distinction between them. This was a major impetus to the further study of autonomic function, providing the morphological basis for all subsequent studies. A student of Gaskell and Langley in Cambridge in the 1890s was Henry Dale, who was strongly influenced by their work, and spent much of his own career investigating autonomic mechanisms. One of his early experiments showed that an injection of adrenaline into an anaesthetized animal produced very similar effect (such as increased arterial blood pressure) to those noticed when sympathetic nerves were stimulated. The significance of the observation was not clear at the time, but it intrigued Dale, who gradually elucidated the relationship between the autonomic nervous system and chemical stimulation by discovering that nerves communicate by the release of specific neurotransmitter chemicals. It was Dale (later Sir Henry) who showed that acetylcholine can stimulate not only autonomic ganglia, but also the synapses of postganglionic parasympathetic fibres (on smooth muscle, heart muscle, and glands), and even ordinary, skeletal muscle. This implies that all these classes of nerve fibres produce acetylcholine as the transmitter substance at their terminals. On the other hand, the receptors on which the acetylcholine acts vary from one system to another. The acetylcholine receptors in the membranes of cells in the autonomic ganglia and of skeletal muscle are called nicotinic because they can be stimulated by the drug nicotine. But those in the membranes of the target cells of postganglionic parasympathetic axons are called muscarinic since they can be activated by muscarine but not by nicotine. The many effects of the drug atropine, or Belladonna, are due to the fact that it blocks muscarinic (but not nicotinic) receptors and hence inhibits the parasympathetic system.
The story is different for transmission at postganglionic sympathetic nerve endings. The main hormone produced by the adrenal medulla, adrenaline (or epinephrine, because of the position of the adrenal glands, above the kidneys — Latin -ren, Greek, nephros) was found to have many effects similar to those resulting from stimulation of the sympathetic system. For some time it was thought that adrenaline was the neurotransmitter released by postganglionic sympathetic fibres, which therefore became known as ‘adrenergic’ nerves. However, there are important differences. We now know that the principal sympathetic transmitter is the related substance noradrenaline (norepinephrine), which is also released as a hormone, along with adrenaline, by the adrenal medulla. The discovery that different drugs can selectively block certain of the actions of adrenaline or noradrenaline led to the view that they act on different receptors in the membranes of the target tissues. Two such types of receptor were distinguished and named alpha- and beta-adrenoceptors; both types were later subdivided. Adrenaline and noradrenaline both act through these, but disproportionately at different sites. One result of such research has been the well-known beta-blocker drugs, used to treat hypertension and heart disease. They bind with beta-adrenoceptors and hence can prevent some of the constriction of blood vessels and stimulation of the heart by sympathetic nerves and the circulating hormones.
It subsequently emerged that some of the effects of sympathetic nerve stimulation cannot be prevented by drugs that block either type of adrenergic transmission. This is because there are other neurotransmitters, with their own specific receptors, operating at sympathetic nerve endings, either alone or in combination with noradrenaline as ‘co-transmitters’.
The work from Dale's laboratory, carried out by physiologists in collaboration with chemists, progressed until his retirement in the late 1930s. Recognition of additional transmitters and of categories of receptors, elucidation of their nature and the consequences of their interaction, are continued by many distinguished contemporary scientists who are unravelling the complexities and diversities of autonomic nervous mechanisms. The powerful techniques of molecular biology are revealing the way in which the genes produce the enzymes that synthesize neurotransmitters and construct the various receptors that they act on.
Sheila Jennett, and E. M. Tansey
See also adrenal glands; membrane receptors; neurotransmitters.
Autonomic Nervous System
Autonomic nervous system
The nervous system responsible for regulating automatic bodily processes, such as breathing and heart rate. The autonomic system also involves the processes of metabolism, or the storage and expenditure of energy.
The nervous system consists of two main structures, the central nervous system (the brain and the spinal cord) and the peripheral nervous system (the sense organs and the nerves linking the sense organs, muscles, and glands to the central nervous system). The structures of the peripheral nervous system are further subdivided into the autonomic nervous system (automatic bodily processes) and the somatic nervous system.
The part of the autonomic nervous system that controls the storage of energy (called anabolism) is the parasympathetic division. Parasympathetic (or anabolic) activities involve bodily functions that occur in normal, nonstressful situations. For example, after eating, the digestive process begins, whereby nutrients are taken from the food and stored in the body. The flow of blood increases to the stomach and intestines while at the same time the heart rate decreases and saliva is secreted. The parasympathetic division also mediates sexual arousal, even though most parasympathetic functions lead to lower overt arousal levels. Sexual climax is controlled by the sympathetic division.
In general, sympathetic processes reverse parasympathetic responses. The sympathetic division is activated when the body mobilizes for defense or in response to stress . Such processes use energy stored during anabolism; this use of energy is referred to as catabolism. In defensive situations, the heart rate increases, the lungs expand to hold more oxygen, the pupils dilate, and blood flows to the muscles.
While the autonomic nervous system normally functions quite appropriately, abnormalities can appear. In anxiety disorders, for example, certain somatic (bodily) symptoms such as muscular tension, hyperventilation, increased heart rate, and high blood pressure are increased, posing the body for attack. This physiological response can lead to such additional maladies as headaches and digestive problems. At times, parasympathetic responses occur simultaneously. In extreme stressful situations, for example, an individual may experience involuntary discharge of the bladder and bowels. Some research has also indicated deficiencies in autonomic arousal processes in psychiatric patients prior to schizophrenic breakdown.
For decades, scientists believed that autonomic processes were not amenable to voluntary control. In recent years, however, people with heart problems have learned to modify heart rates, and headache sufferers have learned to modify blood flow to relieve pain through biofeedback techniques.
Biofeedback and Behavioral Medicine. New York: Aldine Pub. Co., published annually since 1981.