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The ANS system is divided into 2 systems called the sympathetic and the parasympathetic divisions. The Sympathetic system is also known as the"fight-or-flight response" and the Parasympathetic is referred to as the " Rest and digest" division.

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Sympathetic Division's Neurotransmitters

Norepinephrine

Epinephrine

Parasympathetic Division's Neurotransmitters

Acetylcholine

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Location for the Sympathetic division's neurotransmitters

Lateral gray column of the spinal cord

Location for the Parasympathetic division's neurotransmitters

Postganglionic neurons

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The receptors for the Sympathetic division and their locations

Alpha and Beta receptors

Alphas are located in smooth muscles

Betas are located in cardiac and smooth muscles

The receptors for the Parasympathetic division and their locations

Muscarinic and Nicotinic receptors

Muscarinic receptors are located in the brain

Nicotinic receptors are located in the neuromuscular junctions

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The end organ responses for the Sympathetic division

When the sympathetic division is activated

Heart- heart rate begins to speed up and pushes more blood around the body

Lungs- bronchodilation occurs

Eyes- pupils dilate and allows more light to enter the eyes

When the parasympathetic division is activated

Heart- heart rate slows down and blood pressure begins to lower

Lungs- bronchoconstriction occurs which slows down breathing

Digestive tract- increases the rate of digestion

Eyes- pupils constrict to limit the amount of light that enters the eyes

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Drug Classifications

Cholinomimetics/Cholinesterase antagonists (Parasympathetic drugs)

Anticholinergics (Parasympathetic drugs)

Adrenoreceptor agonists/Sympathomimetics (Sympathetic drugs)

Adrenoreceptor antagonists (Sympathetic drugs)

Receptors Affected

Cholinomimetics/Cholinesterase antagonists

They affect Acetylcholine receptors.

The action of the drugs are to inhibit choline esterase and to protect acetylcholine from hydrolysis.

Anticholinergics

They affect Acetylcholine receptors.

The action of the drugs are to block or decrease the amount of work acetylcholine has on the smooth muscle cells.

Adrenoreceptor agonists/Sympathomimetics

They affect the alpha and beta receptors.

The action of the drugs is to stimulate the beta and alpha receptors.

Adrenoreceptor antagonists

They effect the alpha receptors.

The action of the drug is the block the alpha-1 to help with hypertension.

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Drug names for Cholinesterase antagonist

donepezil (Aricept™)

Drug names for Anticholinergics

dicyclomine (Bentyl™)

Drug names for Adrenoreceptors

albuterol (Ventolin™)

Drug names for Adrenoreceptor antagonist

doxazosin (Cardura XL™)

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I just took anatomy last semester so I used my PowerPoints for that class for most of this information but I will source out the information I used to find the drugs.

https://www.ncbi.nlm.nih.gov/books/NBK538180/

https://www.ncbi.nlm.nih.gov/books/NBK548287/

https://www.ncbi.nlm.nih.gov/books/NBK546597/

https://www.ncbi.nlm.nih.gov/books/NBK538163/

https://pubmed.ncbi.nlm.nih.gov/31644028/

https://www.ncbi.nlm.nih.gov/books/NBK548719/

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Continuing Education Activity

The basis of autonomic pharmacology reflects the physiology of the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) to regulate involuntary reactions to stresses on multiorgan systems within the body. When a pathologic process is present that affects the homeostasis achieved between the SNS and PSNS in this process, either of these branches can become overactive while the other is excessively inhibited. This activity outlines the indications, mechanism of action, safe administration, adverse effects, contraindications, toxicology, and monitoring of the broad array of physiological possibilities when using autonomic pharmacology.

Objectives:

Identify the four major classes of pharmacological agents in autonomic pharmacology.

Summarize the mechanism of action of each of the four main categories of autonomic pharmacological agents.

Review the side effects of each of the four classes of autonomic pharmacological agents.

Outline interprofessional team strategies for improving care coordination and communication to advance appropriate clinical outcomes with these classes of medications, leading to optimal patient outcomes.

Access free multiple choice questions on this topic.
Indications

The basis of autonomic pharmacology reflects the physiology of the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) to regulate involuntary reactions to stresses on multiorgan systems within the body. When a pathologic process is present that affects the homeostasis achieved between the SNS and PSNS in this process, either of these branches can become overactive while the other is excessively inhibited.[1] This break in homeostasis results in various clinical manifestations that can range in severity from simply presenting rhinorrhea symptomology to fatal presentations like cardiovascular collapse.[2] For a wide range of presentations and severity of pathologies, the agents classified in autonomic pharmacology are indicated to re-establish the homeostasis that the human body attempts to produce via the autonomic nervous system (ANS).[3]

Within autonomic pharmacology, there are four specific categories of drugs based on how they affect the ANS:

1. Cholinomimetics/cholinesterase antagonists

2. Adrenoreceptor agonists/sympathomimetics

3. Adrenoreceptor antagonists

The clinical indications of medications from each of the four categories are listed below. Important to note is that this is not a complete list due to the vastness of this topic; the drugs included are representative of each category.

FDA-labeled indications:

Cholinomimetics/Cholinesterase antagonists[4][5][6][7]:

Atropine - used in ACLS guidelines to correct bradyarrhythmias and in ophthalmic surgery as a retinal dilator

Ipratropium and tiotropium - correct acute exacerbations of bronchospasm (asthma, COPD), as well as exacerbation prophylaxis for those conditions

Scopolamine - prevents motion sickness and postoperative nausea/vomiting

Oxybutynin - urge incontinence and postoperative bladder spasm

Dicyclomine, glycopyrrolate - can be used for reducing diarrhea output in irritable bowel syndrome; glycopyrrolate can also be added to cholinesterase reversal of neuromuscular blockades in postoperative anesthesia care to prevent bronchospasm and is currently undergoing investigation as an adjunct treatment in COPD

Clonidine - used as an antihypertensive

Dobutamine, phenylephrine, epinephrine - used to correct severe hypotension in cardiogenic shock and acute heart failure exacerbation; epinephrine specifically also used in ACLS guidelines for non-shockable heart rhythms in cardiac arrest and rapid reversal of fatal anaphylactic reactions

Albuterol - fast-acting bronchodilator used in acute asthma exacerbations

Fenoldopam - corrects hypertension

Bromocriptine - involved in the maintenance of Parkinson disease and conditions involving prolactinoma

Adrenoreceptor antagonists[22][23][24]:

Phenoxybenzamine, phentolamine - used to correct high catecholamine states

Prazosin, doxazosin, terazosin, tamsulosin - indicated to correct urinary retention in benign prostatic hyperplasia

Beta-blockers (propranolol, metoprolol, labetalol, etc.) - indicated for many cardiovascular conditions since they are in the classification of class II antiarrhythmics; these agents are used to manage tachyarrhythmias, hypertension, angina, heart failure, and migraine prophylaxis

Mechanism of Action

As with the homeostasis established via processes performed by the SNS and PSNS, drugs from each of the four categories listed above also work inversely to each other. The primary mechanism of action for most of these agents are to serve as either agonists or antagonists of specific receptors within these systems.[2] The receptors with their locations and physiologic actions are listed below.

For adrenoreceptors stimulated by norepinephrine (synapses) and epinephrine (endocrine), involved in SNS processes[25][26]:

Alpha-1 (A1) - located mostly in postsynaptic effector cells found in smooth muscle; effects mediated by IP3/DAG path, include mydriasis due to contraction of radial muscles, constriction of arteries and veins, urinary retention due to internal/external urethral sphincter contraction, and a decrease in renin release from renal juxtaglomerular cells

Alpha-2 (A2) - located in presynaptic adrenergic terminals found in lipocytes and smooth muscle; effects mediated by decreasing cAMP, including a decrease in norepinephrine release, stimulates platelet aggregation and decreases insulin secretion

Beta-1 (B1) - located in postsynaptic effector cells in the SA node of the heart, lipocytes, brain, juxtaglomerular apparatus of renal tubules, and the ciliary body epithelium; effects mediated by increasing cAMP, including increased heart rate and the conduction velocity through the cardiac nodes, also increases renin release from renal juxtaglomerular cells

Beta-2 (B2) - located in postsynaptic effector cells in smooth muscle and cardiac myocytes; effects mediated by increasing cAMP, include vasodilation, bronchiole dilation, increased insulin secretion, and uterine relaxation

Beta-3 (B3) - located in postsynaptic effector cells in lipocytes and myocardium; similar effects to beta-1 receptors mediated by increasing cAMP

For cholinoreceptors stimulated by acetylcholine, most involved in PSNS processes[27]:

Muscarinic-1 (M1) - important to note is the only cholinoreceptor involved in an SNS process, located in sweat glands of the skin; effects mediated by IP3/DAG path, include glandular contraction and increased secretion

Muscarinic-2 (M2) - located in SA and AV nodes and myocardium; effects mediated by decreasing cAMP, include decreasing heart rate and myocardial conduction velocity

Muscarinic-3 (M3) - located in the smooth muscle of various organ systems; effects mediated by IP3/DAG path, include contraction of the ciliary muscle causing miosis, contraction of bronchioles, increased bronchiole secretions, increased GI motility, detrusor muscle contraction, and internal/external urethral sphincter relaxation

Muscarinic-4 (M4) and Muscarinic (M5) - located primarily in the CNS, e.g., forebrain and substania nigra, respectively

Nicotinic-N (NN) - located in postsynaptic dendrites of both sympathetic and parasympathetic postganglionic neurons; effects mediated by Na+/K+ depolarization, include increased neurotransmission

Nicotinic-M (NM) - located in neuromuscular endplates of skeletal muscle; effects mediated by Na+/K+ depolarization, include skeletal muscle contraction

For dopamine receptors, most involved in both SNS and PSNS processes[28]:

Dopamine 1-5 (D1-5) - located in the CNS, except for Dopamine-1 receptors, which also appear in renal vasculature; effects mediated by cAMP path, include renal artery vasodilation, increased renal blood flow, and modulation of neuroendocrine signaling

Administration

Adverse Effects

Contraindications

Based on the adverse reaction profiles of each category, several significant contraindications can be elucidated[34][35][31]:

Enhancing Healthcare Team Outcomes

Glaucoma - ocular telemetry sensors can help to continuously monitor intraocular pressure.

Shock - requires several monitoring functions as listed:

Maintaining a MAP of 65 and above

MAP measurements via an arterial line

Pulse pressure variation to guide fluid therapy

Bedside echocardiography to assess chambers of the heart and looking for cardiogenic shock vs. obstructive shock (massive PE) and calculate cardiac output/ejection fraction

Pulse index continuous cardiac output (PiCCO) device which can serve to continuously monitor continuous cardiac output and assess fluid response

Asthma/COPD - pulmonary function testing is the standard to diagnose and monitor the severity of pulmonary obstruction; can also evaluate the effectiveness of inhaled autonomic agents in reversing obstructive processes

Arrhythmias - for acute monitoring 4-lead ECG and 12-lead EKG are standard for monitoring tachycardias or bradycardias; if extended monitoring is required extended continuous ambulatory rhythm monitors (ECAM) is the monitoring modality of choice

Physicians, nurses, and pharmacists need to work collaboratively when using medications that interact with the autonomic nervous system to make sure that the pharmacotherapy is safe and effective for each patient. [Level V]

References

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The basis of autonomic pharmacology reflects the physiology of the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) to regulate involuntary reactions to stresses on multiorgan systems within the body. When a pathologic process is present that affects the homeostasis achieved between the SNS and PSNS in this process, either of these branches can become overactive while the other is excessively inhibited.