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The ANS, or autonomic nervous system, has 2 main divisions--The sympathetic and the parasympathetic divisions.

The sympathetic (adrenergic) division is also known as the "flight-or-fight" division.

The parasympathetic (cholinergic) division is also known as the "feed-or-breed" division.

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Autonomic Nervous System Definition

The autonomic nervous system (ANS) is a complex set of neurons that mediate internal homeostasis without conscious intervention or voluntary control. Cells of the ANS innervate all viscera and influence their activity locally as well as mediate global changes to the metabolic state of the organism. The ANS maintains blood pressure, regulates the rate of breathing, influences digestion, urination, and modulates sexual arousal.

Anatomy of the Autonomic Nervous System

The autonomic nervous system contains two types of neurons that interact with each other at ganglia near the spinal cord. The initial preganglionic neurons begin at the central nervous system in different parts of the spinal cord. These preganglionic neurons form synapses with postganglionic neurons at ganglia that decorate either side of the spinal cord. The postganglionic neuron forms a synapse with effector cells.

There are two main branches to the ANS - the sympathetic nervous system and the parasympathetic nervous system. The neurons of the sympathetic nervous system emerge from the thoracic and lumbar regions of the spinal cord, while the parasympathetic neurons are associated with the cranial and sacral regions. The sympathetic nervous system is usually activated in response to emergencies, especially those that threaten survival. On the other hand, the parasympathetic response is related to enhancing growth and reproduction.

Functions of the Autonomic Nervous System

The autonomic nervous system controls the cardiovascular system. It can alter the force and rate of heart contractility, as well as the constriction and dilation of blood vessels. Therefore, it also influences blood pressure. The rate of breathing can also be changed by the ANS. It affects both skeletal and smooth muscle fibers across the body, whether it is changing the metabolism of glucose in skeletal muscles or causing pupil dilation in the eye. The ANS can influence digestive efficiency, altering the secretion of enzymes from glands and the rate of peristaltic movement. For instance, activation of the sympathetic nervous system slows down digestion and diverts blood flow towards skeletal muscle. It can impair sexual arousal and shut down most non-essential functions of the body. On the other hand, the parasympathetic nervous system enhances digestive secretions, peristaltic movements, encourages normal cycles of circadian activity, deep sleep and activates the repair mechanisms of the body. In most cases, a physiological response by the parasympathetic nervous system is in direct opposition to the results mediated by the sympathetic nervous system. Colloquially, the sympathetic nervous system is said to influence the fight-or-flight response, and the parasympathetic nervous system is related to the feed-and-breed, or rest-and-digest responses.

Involuntary actions like sneezing, swallowing or vomiting are also controlled by the ANS. There is evidence that the autonomic nervous system not only influences sexual arousal, but also plays a crucial role in maintaining pregnancy and inducing labor. Finally, the autonomic nervous system also changes urinary output and frequency of micturition.

Examples of the Autonomic Nervous System Response

The autonomic nervous system is often described using the response to imminent physical danger and the recovery of the body after the threat has receded. For instance, when faced with a predator, the body increases heart rate and breathing, reduces digestive secretions and activity, and preferentially diverts blood towards skeletal muscles to enable the body to physically combat the challenge. This is usually accompanied by piloerection to conserve body heat. This is why the sympathetic nervous system is said to mediate the fight-or-flight response. Once the situation has become calmer, the parasympathetic nervous system restores the body towards normal functioning, resuming digestion and excretion, reducing blood pressure and restoring normal circadian rhythms.

However, even in the absence of an external threat, the two branches of the autonomic nervous system undergo changes, and interact closely with the endocrine system to minutely monitor the internal and external environment. For instance, sympathetic activation can lead to an increase in circulating plasma levels of epinephrine and norepinephrine secreted from the adrenal gland. On the other hand, hormones can alter the ANS response as well. In fertile, reproducing mammalian females, this interaction between the ANS and the endocrine systems is particularly interesting. Estrogen is involved in increasing the activity of a crucial part of the parasympathetic nervous system - the vagus nerve. Estrogen simultaneously damps sympathetic nervous system activity while progesterone appears to have the opposite effect. This can be seen in the basal level of heart rate variability (HRV). Usually, heart rate increases during inspiration and decreases during expiration. This variation is normal and is influenced by the vagus nerve. When heart rate variability decreases, it indicates reduced parasympathetic activity. In the follicular phase, under the influence of increased plasma estrogen concentrations, there seems to be an increase in parasympathetic nervous activity affecting HRV. On the other hand, during the luteal phase, HRV points towards a decrease in vagal activity, and a shift in the sympathovagal balance. The importance of these changes to the cardiovascular microenvironment is not fully understood, but it is hypothesized that this could explain the differences in the risk faced by men and women for heart disease. However, it is important to note that gross cardiovascular parameters such as blood pressure or heart rate remain mostly unaffected by the phase of the menstrual cycle due to other compensatory mechanisms.

The interaction between the ANS and cardiovascular system becomes even more important during pregnancy as there are large-scale changes to hemodynamics. Blood volume, basal oxygen consumption, red cell mass, cardiac output, and the heart rate increase in pregnant women. Both systolic and diastolic blood pressure drop and there is extensive remodeling of all blood vessels. While the changing hormonal environment primarily mediates these changes, the ANS is also an important player. Here again, HRV becomes a relatively sensitive and non-invasive measure of ANS activity. Studying the variability in heart rate of pregnant women at different gestational ages points towards an increase in vagal activity in the first trimester, coupled with a decrease in sympathetic nervous system activation. This reverses as gestational age increases, with great spikes in neural activity of the sympathetic nervous system and the release of adrenal hormones - both from the cortex and medulla - as the woman nears term.

After birth, lactation is influenced mostly by the sympathetic nervous system (SNS), since there is very little evidence of parasympathetic innervation of mammary glands. While hormones like oxytocin are important for the stimulation of milk production, activation of the SNS can alter the response of the body to the hormone. Norepinephrine can inhibit blood flow to the mammary glands, inhibit their response to oxytocin, as well as directly influence the release of the hormone from the central nervous system. While these effects have been better studied in cows, there is anecdotal evidence to support this interrelationship in humans as well.

Ganglion - In neurobiology, refers to a cluster of neural cell bodies consisting of soma and dendrites. Different cells within ganglia are linked to each other through synapses, different ganglia interact to form a plexus.

Piloerection - Involuntary bristling of hair on the body, usually in response to cold, or fear. Commonly called goosebumps.

Plexus - Branching network of interconnecting nerves or ganglia, that can innervate a relatively large area within the body.

Soma - Bulbous cell body of a neuron, containing the nucleus.

Quiz

1. Which of these statements about the autonomic nervous system is true?
A. Not under voluntary control
B. Influences the cardiovascular system
C. Interacts with the endocrine system
D. All of the above

2. Which of these statements about the vagus nerve is true?
A. Important part of the sympathetic nervous system
B. Increases heart rate variability
C. Increased activity during the third trimester of pregnancy
D. All of the above

3. A group of surgeons is working hard on a liver transplant. The procedure lasts for over 12 hours during which time they were mostly standing, focusing deeply, and looking intently at the surgical surfaces. If it was possible to measure their physiological parameters, which of these changes would be seen in their bodies?
A. Increased conversion of glucose to glycogen in their skeletal muscles
B. Constriction of pupils
C. Changes to melatonin levels
D. All of the above

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Autonomic Nervous System - Definition, Function & Examples | Biology Dictionary

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The autonomic nervous system (ANS) is a complex set of neurons that mediate internal homeostasis without conscious intervention or voluntary control. Cells of the ANS innervate all viscera and influence their activity locally as well as mediate global changes to the metabolic state of the organism.

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Neurotransmitters & The Receptors They Love

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Neurotransmitters & The Receptors They Love

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There are 4 major neurotransmitters that are released in the ANS.

The cholinergic fibers which include all ANS preganglionic axons and all parasympathetic postganglionic axons at synapses with their effectors release acetylcholine (ACh).

The adrenergic fibers which include the majority of sympathetic postganglionic axons release norepinephrine (NE). An exception is sympathetic postganglionic fibers that secrete ACh onto eccrine sweat glands.

Another adrenergic neurotransmitter is epinephrine (EPI) which is produced by the adrenal medulla and acts on adrenergic receptors.

The 4th major neurotransmitter in the ANS is dopamine (DA) which is a precursor to NE and stimulates alpha, beta, & dopaminergic receptors. The effects vary based on the amount of the neurotransmitter at the receptor.

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ANS.pptx - Figure 14.2 Comparison of Motor Neurons in the Somatic and Autonomic Nervous Systems (1 of 2) | Course Hero

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View ANS.pptx from BIO 201 at University Of Arizona. Figure 14.2 Comparison of Motor Neurons in the Somatic and Autonomic Nervous Systems (1 of 2)

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1. Adrenal medulla releases epinephrine

2. Arteries-vasoconstriction (except for coronary & skeletal muscle arteries which are dilated)

3. Heart- Increases heart rate (+chronotropic), AV conduction (+dromotropic), and contractility (+inotropic)

4. GI Tract- decreased motility, decreased secretions

5. Pupil of the eye- Mydriasis

6. Respiratory passages (lower)- bronchodilation

7. Urinary bladder- relaxation

8. Urinary sphincter- contraction

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1. Arteries-Most arteries not supplied by parasympathetic nerves.

2. Heart- Decreased heart rate (- chronotropic), AV conduction (- dromotropic), and contractility (- inotropic)

3. GI Tract- increased motility, increased secretions

4. Pupil of the eye- miosis

5. Respiratory passages (lower)- bronchoconstriction

6. Urinary bladder- contraction

7. Urinary sphincter- relaxation

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Sympathomimetic and Sympatholytic Drug Classes & Their Effects

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Sympathomimetic and Sympatholytic Drug Classes & Their Effects

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Sympathetic Nervous System Drug Classifications:

Alpha-1 Adrenergic Agonists: Alpha-1 receptor stimulated: Contraction of smooth muscle, vasoconstriction=increased BP, vasoconstriction in nasal passages=decongestant effect.

Adrenergic Agonists: All alpha and beta receptors stimulated: causes vasoconstriction, increases BP, cardiac stimulant, and a bronchodilator.

Alpha-1 Adrenergic Antagonists: Binds to alpha-1 receptors and blocks other substances from binding. Causes relaxation of smooth muscle, vasodilation=decreased BP, increases urine flow by relaxing smooth muscle of ureters.

Beta-1 Adrenergic Agonists: {Dose dependent MOA/Effects} Low Dose: stimulates dopaminergic (d-1) receptors in kidneys causing vasodilation and increases renal blood flow. Moderate Dose: Beta-1 receptors are stimulated: causes + inotropic effect and increased cardiac output. High Dose:  Alpha-1 receptors are stimulated: causes vasoconstriction=increased BP.

Beta-2 Adrenergic Agonists: Beta-2 receptors stimulated: causes relaxation of smooth muscle in the lungs (=bronchodilation) and of the uterus.

Selective Beta-1 Adrenergic Antagonists ("Beta Blockers"): Beta-1 receptor blocked (EPI and NE effects antagonized): causes negative inotropic effect (=decreased cardiac output=decreased BP), negative chronotropic effect, & negative dromotropic effect.

Non-selective Beta Antagonists ("Beta Blockers"): Blocks both beta-1 and beta-2 receptors: causes negative inotropic effect (=decreased cardiac output=decreased BP), negative chronotropic effect, & negative dromotropic effect. ALSO can cause bronchoconstriction. Contraindicated for asthma/respiratory disease patients.

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Parasympathomimetic and Parasympatholytic Drug Classes & Their Effects

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Parasympathomimetic and Parasympatholytic Drug Classes & Their Effects

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Parasympathetic Nervous System Drug Classifications:

Direct-Acting Cholinergic Agonists: Directly bind to the muscarinic receptors in parasympathetic division and mimics ACh: causes miosis, decreases intraocular pressure, increases GI motility and urination.

Indirect-Acting Cholinergic Agonists: Inhibit the enzyme that breaks down ACh (acetylcholinesterase), increases ACh: Causes increased digestion/GI motility and urination, negative chronotropic/inotropic/dromotropic effects.

Anticholinergics: Binds to cholinergic receptors (competitive antagonism): causes  + chronotropic effect, decrease Vagus Nerve activity, mydriasis, slows digestions/GI motility and urination.

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Alpha-1 Adrenergic Agonists:
ephedrine
phenylephrine (Neo-Synephrine®)

Adrenergic Agonist:
epinephrine (Adrenalin®)

Beta-1 Adrenergic Agonist:
dobutamine

Beta-2 Adrenergic Agonists:
formoterol (Foradil®)
albuterol (Proventil®/Ventolin®)
terbutaline (Brethine®)

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Alpha-1 Adrenergic Antagonists:
prazosin (Minipress®)
terazosin (Hytrin®)
doxazosin (Cardura®)

Non-Selective Beta Adrenergic Antagonist:
nadolol (Corgard®)
propanolol (Inderol®)
timolol (Blocadren®)

Selective Beta Adrenergic Antagonist:
atenolol (Tenormin®)
metoprolol (Lopressor®)

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Direct-Acting Cholinergic Agonists:
acetylcholine
pilocarpine (Pilocar®)
bethanechol (Urecholine®)

Indirect-Acting Cholinergic Agonists:
neostigmine (Prostigmin®)

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Anticholinergics:
atropine
dicyclomine (Bentyl®)