Synapses between the autonomic postganglionic neuron and effector tissue—the neuroeffector junction—differ greatly from neuron-to-neuron synapses. The postganglionic fibers in the ANS do not terminate in a single swelling like the synaptic knob, nor do they synapse directly with the cells of a tissue.
Instead, where the axons of these fibers enter a given tissue, they contain multiple swellings called varicosities. When the neuron is stimulated, these varicosities release neurotransmitters along a significant length of the axon and, therefore, over a large surface area of the effector tissue.
The neurotransmitter diffuses through the interstitial fluid to wherever its receptors are located in the tissue. This diffuse release of the neurotransmitter affects many tissue cells simultaneously. Furthermore, cardiac muscle and most smooth muscle have gap junctions between cells. These specialized intercellular communications allow for the spread of electrical activity from one cell to the next.
As a result, the discharge of a single autonomic nerve fiber to an effector tissue may alter the activity of the entire tissue. The ANS is composed of 2 anatomically and functionally distinct divisions, the sympathetic system and the parasympathetic system. Both systems are tonically active.
In other words, they provide some degree of nervous input to a given tissue at all times. Therefore, the frequency of discharge of neurons in both systems can either increase or decrease.
As a result, tissue activity may be either enhanced or inhibited. This characteristic of the ANS improves its ability to more precisely regulate a tissue's function.
Without tonic activity, nervous input to a tissue could only increase. Many tissues are innervated by both systems. Because the sympathetic system and the parasympathetic system typically have opposing effects on a given tissue, increasing the activity of one system while simultaneously decreasing the activity of the other results in very rapid and precise control of a tissue's function.
Each system is dominant under certain conditions. The overall effect of the sympathetic system under these conditions is to prepare the body for strenuous physical activity. More specifically, sympathetic nervous activity will increase the flow of blood that is well-oxygenated and rich in nutrients to the tissues that need it, in particular, the working skeletal muscles.
The parasympathetic system predominates during quiet, resting conditions. The overall effect of the parasympathetic system under these conditions is to conserve and store energy and to regulate basic body functions such as digestion and urination. The preganglionic neurons of the sympathetic system arise from the thoracic and lumbar regions of the spinal cord segments T 1 through L 2.
Most of these preganglionic axons are short and synapse with postganglionic neurons within ganglia found in the sympathetic ganglion chains. These ganglion chains, which run parallel immediately along either side of the spinal cord, each consist of 22 ganglia. The preganglionic neuron may exit the spinal cord and synapse with a postganglionic neuron in a ganglion at the same spinal cord level from which it arises.
The preganglionic neuron may also travel more rostrally or caudally upward or downward in the ganglion chain to synapse with postganglionic neurons in ganglia at other levels.
In fact, a single preganglionic neuron may synapse with several postganglionic neurons in many different ganglia. Overall, the ratio of preganglionic fibers to postganglionic fibers is about The long postganglionic neurons originating in the ganglion chain then travel outward and terminate on the effector tissues.
This divergence of the preganglionic neuron results in coordinated sympathetic stimulation to tissues throughout the body. The concurrent stimulation of many organs and tissues in the body is referred to as a mass sympathetic discharge.
Other preganglionic neurons exit the spinal cord and pass through the ganglion chain without synapsing with a postganglionic neuron. Instead, the axons of these neurons travel more peripherally and synapse with postganglionic neurons in one of the sympathetic collateral ganglia.
These ganglia are located about halfway between the CNS and the effector tissue. Finally, the preganglionic neuron may travel to the adrenal medulla and synapse directly with this glandular tissue. The cells of the adrenal medulla have the same embryonic origin as neural tissue and, in fact, function as modified postganglionic neurons. Instead of the release of neurotransmitter directly at the synapse with an effector tissue, the secretory products of the adrenal medulla are picked up by the blood and travel throughout the body to all of the effector tissues of the sympathetic system.
An important feature of this system, which is quite distinct from the parasympathetic system, is that the postganglionic neurons of the sympathetic system travel within each of the 31 pairs of spinal nerves. This allows for the distribution of sympathetic nerve fibers to the effectors of the skin including blood vessels and sweat glands. In fact, most innervated blood vessels in the entire body, primarily arterioles and veins, receive only sympathetic nerve fibers.
Therefore, vascular smooth muscle tone and sweating are regulated by the sympathetic system only. In addition, the sympathetic system innervates structures of the head eye, salivary glands, mucus membranes of the nasal cavity , thoracic viscera heart, lungs and viscera of the abdominal and pelvic cavities eg, stomach, intestines, pancreas, spleen, adrenal medulla, urinary bladder.
The preganglionic neurons of the parasympathetic system arise from several nuclei of the brainstem and from the sacral region of the spinal cord segments S 2 -S 4. The axons of the preganglionic neurons are quite long compared to those of the sympathetic system and synapse with postganglionic neurons within terminal ganglia which are close to or embedded within the effector tissues.
The axons of the postganglionic neurons, which are very short, then provide input to the cells of that effector tissue. The preganglionic neurons that arise from the brainstem exit the CNS through the cranial nerves. The occulomotor nerve III innervates the eyes; the facial nerve VII innervates the lacrimal gland, the salivary glands and the mucus membranes of the nasal cavity; the glossopharyngeal nerve IX innervates the parotid salivary gland; and the vagus nerve X innervates the viscera of the thorax and the abdomen eg, heart, lungs, stomach, pancreas, small intestine, upper half of the large intestine, and liver.
The preganglionic neurons that arise from the sacral region of the spinal cord exit the CNS and join together to form the pelvic nerves. These nerves innervate the viscera of the pelvic cavity eg, lower half of the large intestine and organs of the renal and reproductive systems. Because the terminal ganglia are located within the innervated tissue, there is typically little divergence in the parasympathetic system compared to the sympathetic system.
In many organs, there is a ratio of preganglionic fibers to postganglionic fibers. Therefore, the effects of the parasympathetic system tend to be more discrete and localized, with only specific tissues being stimulated at any given moment, compared to the sympathetic system where a more diffuse discharge is possible.
The 2 most common neurotransmitters released by neurons of the ANS are acetylcholine and norepinephrine. Neurotransmitters are synthesized in the axon varicosities and stored in vesicles for subsequent release. Nerve fibers that release acetylcholine are referred to as cholinergic fibers. These include all preganglionic fibers of the ANS, both sympathetic and parasympathetic systems; all postganglionic fibers of the parasympathetic system; and sympathetic postganglionic fibers innervating sweat glands.
Nerve fibers that release norepinephrine are referred to as adrenergic fibers. Most sympathetic postganglionic fibers release norepinephrine.
As previously mentioned, the cells of the adrenal medulla are considered modified sympathetic postganglionic neurons. Instead of a neurotransmitter, these cells release hormones into the blood. Unlike true postganglionic neurons in the sympathetic system, the adrenal medulla contains an enzyme that methylates norepinephrine to form epinephrine. The synthesis of epinephrine, also known as adrenaline, is enhanced under conditions of stress. These 2 hormones released by the adrenal medulla are collectively referred to as the catecholamines.
For any substance to serve effectively as a neurotransmitter, it must be rapidly inactivated or removed from the synapse or, in this case, the neuroeffector junction.
This is necessary in order to allow new signals to get through and influence effector tissue function. The primary mechanism used by cholinergic synapses is enzymatic degradation. Acetylcholinesterase hydrolyzes acetylcholine to its component choline and acetate. It is one of the fastest acting enzymes in the body and acetylcholine removal occurs in less than 1 msec.
The most important mechanism for the removal of norepinephrine from the neuroeffector junction is the reuptake of this neurotransmitter into the sympathetic nerve that released it. Norepinephrine may then be metabolized intraneuronally by monoamine oxidase MAO.
The circulating catecholamines, epinephrine and norepinephrine, are inactivated by catechol-O-methyltransferase COMT in the liver. As discussed in the previous section, all of the effects of the ANS in tissues and organs throughout the body, including smooth muscle contraction or relaxation, alteration of myocardial activity, and increased or decreased glandular secretion, are carried out by only 3 substances, acetylcholine, norepinephrine, and epinephrine.
Furthermore, each of these substances may stimulate activity in some tissues and inhibit activity in others. How can this wide variety of effects on many different tissues be carried out by so few neurotransmitters or hormones? The effect caused by any of these substances is determined by the receptor distribution in a particular tissue and the biochemical properties of the cells in that tissue, specifically, the second messenger and enzyme systems present within the cell.
The neurotransmitters of the ANS and the circulating catecholamines bind to specific receptors on the cell membranes of the effector tissue. All adrenergic receptors and muscarinic receptors are coupled to G proteins which are also embedded within the plasma membrane. Receptor stimulation causes activation of the G protein and the formation of an intracellular chemical, the second messenger. The neurotransmitter molecule, which cannot enter the cell itself, is the first messenger.
The function of the intracellular second messenger molecules is to elicit tissue-specific biochemical events within the cell which alter the cell's activity. In this way, a given neurotransmitter may stimulate the same type of receptor on 2 different types of tissue and cause 2 different responses due to the presence of different biochemical pathways within each tissue.
Acetylcholine binds to 2 types of cholinergic receptors. Nicotinic receptors are found on the cell bodies of all postganglionic neurons, both sympathetic and parasympathetic, in the ganglia of the ANS.
The resulting influx of these 2 cations causes depolarization and excitation of the postganglionic neurons the ANS pathways. Muscarinic receptors are found on the cell membranes of the effector tissues and are linked to G proteins and second messenger systems which carry out the intracellular effects. Acetylcholine released from all parasympathetic postganglionic neurons and some sympathetic postganglionic neurons traveling to sweat glands binds to these receptors.
Muscarinic receptors may be either inhibitory or excitatory, depending on the tissue upon which they are found. For example, muscarinic receptor stimulation in the myocardium is inhibitory and decreases heart rate while stimulation of these receptors in the lungs is excitatory, causing contraction of airway smooth muscle and bronchoconstriction.
All of these receptors are linked to G proteins and second messenger systems which carry out the intracellular effects. Alpha receptors are the more abundant of the adrenergic receptors. Alpha one receptor stimulation leads to an increase in intracellular calcium. As a result, these receptors tend to be excitatory. Hypertension, or a chronic elevation in blood pressure, is a major risk factor for coronary artery disease, congestive heart failure, stroke, kidney failure, and retinopathy.
An important cause of hypertension is excessive vascular smooth muscle tone or vasoconstriction. Alpha 2 receptor stimulation causes a decrease in cAMP and, therefore, inhibitory effects such as smooth muscle relaxation and decreased glandular secretion. In this way, norepinephrine inhibits its own release from the sympathetic postganglionic neuron and controls its own activity. Whether this results in an excitatory or an inhibitory response depends upon the specific cell type.
Beta 2 receptors tend to be inhibitory. Beta 2 receptors have a significantly greater affinity for epinephrine than for norepinephrine. Furthermore, terminations of sympathetic pathways are not found near these receptors. Beta 1 receptors are also found on certain cells in the kidney. Stimulation of these receptors, which have a stronger affinity for norepinephrine, causes lipolysis.
Sympathomimetic drugs are those that produce effects in a tissue resembling those caused from stimulation by the sympathetic nervous system. An important use for these drugs is in the treatment of bronchial asthma which is characterized by bronchospasm. Therefore, in patients with bronchospasm, an undesirable side effect of treatment with these non-selective agents is an increase in heart rate.
They are equally effective in causing bronchodilation with a much lower risk of adverse cardiovascular effects. The 2 divisions of the ANS are dominant under different conditions.
As such, the physiological effects caused by each system are quite predictable. In other words, all of the changes in organ and tissue function induced by the sympathetic system work together to support strenuous physical activity and the changes induced by the parasympathetic system are appropriate for when the body is resting.
Parasympathetic stimulation causes mainly opposite effects—decreased heart rate and strength of contraction. To express these effects in another way, sympa thetic stimulation increases the effectiveness of the heart as a pump, as required during heavy exercise, whereas parasympathetic stimulation decreases heart pumping, allowing the heart to rest between bouts of strenuous activity.
Systemic Blood Vessels. Most systemic blood vessels, especially those of the abdominal viscera and skin of the limbs, are constricted by sympathetic stimulation. Parasympathetic stimulation has almost no effects on most blood vessels except to dilate vessels in certain restricted areas, such as in the blush area of the face. Under some conditions, the beta function of the sym-pathetics causes vascular dilation instead of the usual sympathetic vascular constriction, but this occurs rarely except after drugs have paralyzed the sympathetic alpha vasoconstrictor effects, which, in blood vessels, are usually far dominant over the beta effects.
The arterial pressure is determined by two factors: propulsion of blood by the heart and resistance to flow of blood through the peripheral blood vessels. Sympathetic stimulation increases both propulsion by the heart and resistance to flow, which usually causes a marked acute increase in arterial pressure but often very little change in long-term pressure unless the sympa-thetics stimulate the kidneys to retain salt and water at the same time. Conversely, moderate parasympathetic stimulation via the vagal nerves decreases pumping by the heart but has virtually no effect on vascular peripheral resistance.
Therefore, the usual effect is a slight decrease in arterial pressure. But very strong vagal parasympathetic stimulation can almost stop or occasionally actually stop the heart entirely for a few seconds and cause temporary loss of all or most arterial pressure. Because of the great importance of the sympathetic and parasympathetic control systems, they are discussed many times in this text in relation to multiple body functions.
In general, most of the entodermal structures, such as the ducts of the liver, gallbladder, ureter, urinary bladder, and bronchi, are inhibited by sympathetic stimulation but excited by parasympathetic stimulation.
Sympathetic stimulation also has multiple metabolic effects such as release of glucose from the liver, increase in blood glucose concentration, increase in glycogenolysis in both liver and muscle, increase in skeletal muscle strength, increase in basal metabolic rate, and increase in mental activity.
Finally, the sympathetics and parasympathetics are involved in execution of the male and female sexual acts. Continue reading here: Function of the Adrenal Medullae. Euroform Healthcare. Responses Jesse Does sympathetic stimulation increase blood glucose? Fethawi Does increased parasympathetic ans stimulation increase metabolic rate? Askalu Is sweating considered a sympathetic or parasympathetic resonse? Semere What effect does parasympathetic nervous system have on blood vessels of viscera?
Esmeralda What are effects of sympathetic and parasympathetic stimulation on different organs in the body? Russom Is sweating controlled by parasympathetic system? Nasih What happens to aprarsympathetic system is stimulated?
Jason How sympathetic affect human health? Faith Coelho What is the effect on the kidney of sympathetic stimulation? Mac What happens to sweat glands in parasympathetic nervous system? Scudamor Brockhouse What is the parasympathetic stimulation effect on the lungs?
Kira What effect does the sympathetic nervous system have on your blood vessels? Anastasia Siciliani Why are the eyes constricted in parasympathetic system? Fatima What happens to arterioles in skin when sympathetic system is stimulated?
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