Drugs affecting Autonomic Nervous System Flashcards
Describe “big picture” of human nervous system and name postganglionic neurotransmitters:
Somatic Nervous System –> acetylcholine –> skeletal muscle
Autonomic Nervous System
- Sympathetic –> NorEpinephrine & Epinephrine –> smooth muscle contraction (blood vessels, sphincter, radial muscle of eye)
- Parasympathetic –> acetylcholine –> muscarinic receptors (heart, smooth muscle, glands)
Postganglionic neurotransmitter of the somatic nervous system:
Acetycholine
The postganglionic neurotransmitter of the sympathetic nervous system:
Norepinephrine and Epinephrine
Postganglionic neurotransmitter of the parasympathetic nervous system:
Acetylcholine
Review ANS visual
Review ANS Visual
Effects of sympa/parasympathetic nervous systems
Effects of sympa /parasympathetic nervous systems
What neurotransmitter is responsible for cholinergic effects?
Acetylcholine
What nervous system is acetylcholine release associated with?
Parasympathetic system
What neurotransmitter is associated with anticholinergic effects?
Norepinephrine
What neurotransmitter is associated with the sympathetic nervous system effects?
Norepinephrine
Which nervous system when active is associated with anticholinergic effects?
Sympathetic
Acetylcholine effects pneumonics:
SLUDGE-M
Acetylcholine causes:
S - Salivation
L - Lacrimation
U- Urination
D - Diarrhea
G - GI Motility
E- Emesis (possibly)
M- Miosis (pupil constriction)
Acetylcholine effects pneumonics:
DUMBELS
Acetylcholine causes increased:
D - Diarrhea
U - Urination
M - Miosis (pupil constriction)
B- -Bronchorrhea (constriction)
E - Emesis (possibly)
L - Lacrimation
S - Salivation / Sweating
What does an “agonist” drug do?
Binds to the receptor and cause a change in cellular activity.
“-mimetic”
What does an antagonist drug do?
binds to the receptor, causes no change in cellular activity, and blocks the ability of endogenous substances or other drugs to bind to the receptor.
- -lytic
- Inhibitor
- Blocker
Autonomic Nervous System Terms
- Parasympathetic
- Cholinergic [acetylcholine]
- Muscarinic
- Sympathetic
- Adrenergic [adrenalin]
Autonomic Nervous System Terms
- Parasympathetic
- Cholinergic [acetylcholine]
- Muscarinic
- Sympathetic
- Adrenergic [adrenalin]
What are the usual ending of drugs that are adrenergic agonists?
“-ine”
What is MOA for Adrenergic Agonists?
- Act on adrenergic receptors
- Activates directly/indirectly:
- alpha - adrenergic -
- beta - adrenergic - receptors
- dopaminergic -
(Indirect compounds are usually slower in onset of action and have a longer duration of action)
What class of drug is the treatment of anaphylaxis?
Adrenergic Agonists
(Epi pen)
Adrenergic (post-synaptic) Receptor Stimulation Reminders
(Norepinephrine receptors)
Alpha-1 → one red line (vaso constriction)
Alpha-2 → two red lines (vaso dilation)
Beta-1 → heart (one heart for cardiac stimulation)
Beta-2 →pair of lungs (two lungs - for beta 2, effects bronchodilation, etc)
Adrenergic Receptor Stimulation (post synaptic)
What happens when Alpha-1 receptors are stimulated?
- Vasoconstriction
- Mydriasis
- GI/Bladder contraction
(Think the one red line)
Adrenergic Receptor Stimulation (post synaptic)
What happens when Alpha-2 receptors are stimulated?
Vasodilation (lower BP)
Note that stimulation of Alpha2 receptors creates a negative feedback loop and inhibits sympathetic outflow (aka sympatholytic).
Which postsynaptic adrenergic receptor must be stimulated to produce a sympatholytic effect?
Alpha-2 receptors
Note that stimulation of Alpha2 receptors creates a negative feedback loop and inhibits sympathetic outflow (aka sympatholytic).
Postsynaptic adrenergic receptor stimulation:
Effects of Beta-1
- Cardiac stimulation (increase heart rate, contractility)
(Think drawing one heart for Beta-1, one heart)
Postsynaptic adrenergic receptor stimulation:
Effects of Beta-2
- bronchodilation,
- vasodilation,
- GI relaxation,
- uterine relaxation,
- glycogenolysis (hyperglycemia)
Which adrenergic receptor needs to be stimulated to produce hyperglycemia (glycogenolysis)?
Beta-2
Which adrenergic receptor needs to be stimulated to produce bronchodilation?
Beta-2
Which adrenergic receptor needs to be stimulated to produce GI relaxation?
Beta-2
Which adrenergic receptor needs to be stimulated to produce uterine relaxation?
Beta-2
Which adrenergic receptors needs to be stimulated to produce vasodilation?
Alpha-2 and Beta-2
Which adrenergic receptor needs to be stimulated to produces increased HR and contractility?
Beta-1
When stimulated, which adrenergic receptors can result in lower BP?
Alpha-2 and Beta-2
Which adrenergic receptor needs to be stimulated to produce mydriasis (pupil dilation)?
Alpha-1
Which adrenergic receptor needs to be stimulated to produce vasoconstriction?
Alpha-1
Which adrenergic receptor needs to be stimulated to produce GI/bladder sphincter contraction?
Alpha-1
Effects of adrenergic drugs on eyes:
•Mydriasis (dilate eyes for eye exam)
Effects of adrenergic drugs on respiratory system:
•Cause bronchodilation and manage anaphylactic shock
Effects of adrenergic drug on CV system:
•Improve myocardial contractility, increase in heart rate and blood pressure
Effects of adrenergic drug on GI/GU system:
Decrease peristalsis
Effect of adrenergic drug on the endocrine system:
Increases blood sugar
Effect of adrenergic drug on local anesthetics:
Prolongs anesthetic action
List general ADRs of adrenergic drugs:
Fear
Restlessness
Headache
Tremor
Palpitations
Pallor
Serious ADRs
Stroke
V-Fib
What occurs with Alpha-2 receptor stimulation?
Stimulation of Alpha2 receptors creates a negative feedback loop and inhibits sympathetic outflow (aka sympatholytic).
What are Alpha-2 Adrenergic Agonists - sympathetic effects:
Dry mouth
Constipation
Nausea
GI Upset
What are sympatholytic effects similar to?
Similar to parasympathetic effects:
Bradycardia
Hypotension
(Impotence)
Phenylephrine (Neo-synephrine)
Receptor: Selective Alpha-1 Agonist
Action: Vasopressor
Uses: Treat congestion, hypotension, (uveitis)
Alpha2 Agonists: Clonidine (Catapres)
MOA
MOA: Causes vasodilation by stimulating inhibitory alpha-adrenergic receptors in the brain (centrally)
Alpha2 Agonists: Clonidine (Catapres)
Uses
Lowers blood pressure (2nd or 3rd line) and heart rate
Used for treatment of withdrawal symptoms (ETOH, nicotine, heroin)
Used for attention deficit hyperactivity disorder
Alpha2 Agonists: Clonidine (Catapres)
ADRs
Sedation, dry mouth, and postural hypotension occur but these usually decrease after several weeks of therapy. Sodium and water retention may occur.
Bradycardia, Skin rashes, constipation, urinary retention, impotence, and nightmares may occur.
Abrupt discontinuation of clonidine can result in Rebound Hypertension as soon as 8 and as late as 36 hours after the last dose. Gradually taper over 4 days
Alpha2 Agonists: Clonidine (Catapres)
Rational Drug Selection
Caution in elderly because they are at risk for orthostatic hypotension and fluid retention.
Cat C Pregnancy
What can result with the abrupt discontinuation of an Alpha-2 agonist such as Clonidine (Catapres)
Abrupt discontinuation of clonidine can result in Rebound Hypertension as soon as 8 and as late as 36 hours after the last dose. Gradually taper over 4 days.
Alpha2 Agonists: Methyldopa (Aldomet)
ADRs
Sedation, hepatotoxicity (elevations of transaminase enzymes; fever, malaise & jaundice may occur), development of a positive Coomb’s test (in 10-20% of patients taking 1 g daily for > 6 mo; hemolytic anemia does not occur), flu-like symptoms. Retention of sodium and weight gain may occur during treatment.
Abrupt discontinuation can result in rebound hypertension as soon as 8 and as late as 36 hours after the last dose. Gradually taper over 4 days
Coombs test info:
The direct Coombs test is used to test for autoimmune hemolytic anemia; i.e., a condition of a low count of red blood cells (a.k.a. RBCs) caused by immune system lysis or breaking of RBC membranes causing RBC destruction.
Dobutamine (Dobutrex)
- Receptor: Beta-1
- Use: Cardiac Decompensation
- ADR: Increases heart rate and blood pressure; angina
Beta2 Agonists: Albuterol
MOA and Use
- Relatively selective Beta-2 agonist
- Use: Bronchodilation
Beta2 Agonists: Albuterol
ADRs
•CNS stimulation,
- palpitation,
- tremors ,
- shakiness ,
- hyperactivity ,
- headache , and
- nausea & vomiting .
- May cause irritable behavior in infants
Beta2 Agonists: Albuterol
Rational drug use
- Clinical use in adults and children as young as 4 y/o
- Rational drug selection: Caution: Patients at risk include diabetics, hyperthyroidism, subjects with seizures disorders, and the elderly.
- Excessive use may cause death, cause unknown but probably cardiac arrest. Oral use may delay preterm labor.
Epinephrine (Adrenalin)
Receptors: Alpha 1 & 2; Beta 1 & 2
Uses
- Prolong local anesthetics
- Treat allergic reactions
- CPR
- Status Asthmaticus
Norepinephrine (Levarterenol)
(not needed for test)
- Receptors: Alpha 1; Less Beta 1
- Uses: Treat hypotension
Dopamine (Intropin)
(not needed for test)
- Receptors: Dopamine; Beta-1; Alpha 1 (dose dependent)
- Causes: Renal Vasodilation; Stimulates heart
- Use: Shock syndrome
- ADR: Palpitations, hypotension
Pseudoephedrine & Amphetamine
- Pseudoephedrine (Sudafed)
- Receptors: Alpha & Beta-2
- Uses: Decongestant
- Amphetamine/ Methylphenidate (Ritalin)
- Receptors: Direct and Indirect Adrenergic
- Uses: ADHD; Narcolepsy
- ADR: Nervousness, Insomnia, arrhythmias, tachycardia, headache
- Warnings: HBP; CAD; Glaucoma; Hyperthyroidism; BPH, DM
Another way to think of adrenergic antagonists:
“blockers”
Adrenergic Antagonists
Alpha blockers - discuss:
- Action: block alpha receptors leading to vasodilation
- Used to treat HTN, benign prostatic hyperplasia (BPH), Raynaud’s disease, and migraine headaches
- Nonselective (Phentolamine (Regitine))
- Selective Alpha-1- see next slide
Adrenergic Antagonists
Beta blockers - discuss:
- Action: antagonize or block the effects of catecholamines (epi, NE, dopa); decreases heart rate and reduces vascular smooth muscle tone/ resistance
- Drugs can be “selective” to beta1 receptors or “nonselective” to beta1 and beta2 receptors
- Mainly used for HTN and post myocardial infarction (MI)
What do Alpha-1 blockers typically “end in”
“-zosin”
Example:
- Prazosin (Minipress),
- Doxazosin (Cardura),
- Terazosin (Hytrin)
- Used for HTN
- Tamsulosin (Flomax): Used for BPH
Alpha-1 blockers ADRs
Fluid retention,
Orthostatic HTN (plus dry mouth, constipation, urinary retention, etc)
Warning: 1st dose effect
excess postural hypotension that can occur within 30-90 min of the first few doses
The patient will adjust to the medication with successive doses
To avoid: Take at bedtime; start at 1mg and titrate up every 2 weeks
Way to remember- That patient is “dozin” on the floor! Orthostatic hypotension is a side effect of “zosin”.
What do beta blockers usually end-in?
“-olol”
Describe non-selective beta blockers:
Nonselective:
Blocks beta-1 and beta-2
(e.g., propranolol [Inderal]) (
1st generation)
Discuss selective beta blockers:
Selective for beta-1 receptors (e.g., metoprolol [Toprol]) and atenolol [Tenormin]) :
relatively “cardioselective” beta-1 antagonists) (2nd generation)
Discuss combined beta blockers-
Combined Beta blockers (nonselective) with alpha blocking activity:
(e.g., labetalol [Normodyne]) & carvedilol [Coreg]):
Used to reduce the progression on heart failure because they cause vasodilation of the peripheral vasculature; Especially effective in African Americans
Beta blockers ADRs
for both beta-1 and beta-2 blockers
Dizziness,
lethargy/ fatigue,
nightmares,
mental status changes in elderly,
impotence
Beta blockers ADRs
for both beta-1
bradycardia,
reduced cardiac output
precipitation of heart failure
AV heart block and rebound cardiac excitation
(however they are 1st line drugs in certain types of heart failure, given in left ventricular dysfunction).
Beta blockers ADRs
for beta-2 blockers
bronchoconstriction and hypoglycemia
(from inhibition of glycogenolysis)
What can occur with chronic use of beta blockers?
Upregulation of Beta-1 receptors.
Beta blocker warnings and contraindications
DO NOT STOP ABRUPTLY
(life threatening especially in pts with angina and CAD)
Acute discontinuation of beta blockers can result in excess sympathetic activity seen in 24-48 hours, due to an increase in beta receptors (up-regulation) during blockade.
Myocardial ischemia or cardiac arrhythmias may occur.
Can be minimized by withdrawing these drugs gradually (decrease dose by a half every 4 days- can take 1 to 2 weeks).
Contraindicated: (Esp. non-selective) Asthma or any bronchospastic condition, Caution in diabetics- masks hypoglycemic symptoms EXCEPT diaphoresis), Avoid in pregnant & nursing women
How should beta blocker dosages be adjusted in renal patients?
In renal impaired pts be sure to extend the dosage interval.
There is a higher risk of toxicities if the dosing interval is inadequate to allow for drug elimination.
Cholinergic Agonists
also known as:
parasympathomimetics,
muscarinic agonists
Direct-acting cholinergic drugs
◦Prototype: bethanechol (Urecholine)
◦Prototype: pilocarpine (Pilocar)
Indirect-acting cholinergic drugs
◦Cholinesterase inhibitors
◦Peripheral-Acting: Prototype: neostigmine bromide (Prostigmin)
◦Central-Acting: Donepezil (Aricept)
How do muscarinic agonists work?
Muscarinic agonists act directly on postganglionic parasympathetic receptors
(including those cells that have receptors but do not receive parasympathetic innervation, such as some blood vessels).
Discuss derivatives of acetylcholine
Acetylcholine is not a marketed drug because it must be injected and has an extremely short duration of effect.
- Two types of drugs are used: derivatives of acetylcholine carbachol, bethanechol [Urecholine]
- and cholinomimetic alkaloids (pilocarpine).
What does cholinergic drug do for eyes?
•Eyes: Decrease intraocular pressure in glaucoma, miosis
What does cholinergic drug do for the respiratory system?
•Resp: Stimulates secretions in the tracheobronchial tree, produces bronchoconstriction
What does cholinergic drug do for CV system?
•Cardiovascular: Decrease in heart rate and force of contractility is due to cholinergic innervation of the SA and AV nodes and atrial muscle.
What does cholinergic drug do for GI system?
•GI: Increased tone and amplitude of contraction, peristaltic activity, and secretory action.
What does cholinergic drug do for urinary tract?
•Urinary tract: Increase in ureteral peristalsis and contraction of the detrusor muscle.
What does cholinergic drug do for the neuromuscular system?
•Neuromuscular: Treat Myasthenia gravis, Reverse neuromuscular block
List general ADRs of cholinergic drugs:
- GI discomfort: nausea, vomiting, diarrhea, belching, salivation, and intestinal cramps
- Bradycardia
- Bronchoconstriction
Direct-acting cholinergic drugs: Bethanechol (Urecholine)
MOA
MOA:
- Increases tone of detrusor muscle and causes bladder contractions
- Increases tone of the lower esophageal sphincter
Direct-acting cholinergic drugs: Bethanechol (Urecholine)
Clinical Indications
Urinary retention (Post-op & post-partum)
Direct-acting cholinergic drugs: Bethanechol (Urecholine)
ADRs
Initially:
- Abdominal discomfort/ epigastric pain, salivation, flushed skin, sweating, nausea, vomiting, and miosis are common.
Toxic reactions:
- include intense cramping, diarrhea, urination, bradycardia, and bronchoconstriction.
Direct-acting cholinergic drugs: Bethanechol (Urecholine)
Contraindications
COPD,
asthma,
hyperthyroidism,
peptic ulcer
Direct-acting cholinergic drugs: Bethanechol (Urecholine)
Education
Education: To avoid nausea & vomiting, take 1 hour before or 2 hours after meals.
Direct-acting cholinergic drugs: Pilocarpine (Pilopine)
Discuss uses
- Used primarily as an ophthalmic solution in the treatment of open-angle glaucoma where, by contracting the ciliary muscle, outflow of aqueous humor is improved and intraocular pressure reduced within minutes.
- Used also to treat of xerostomia and Sjogren ’s syndrome because it increases salivation.
Indirect-acting cholinergic drugs:
(Acetyl)cholinesterase inhibitors
Names of drugs (prototypes)
•Prototype: neostigmine bromide (Prostigmin);
Also use pyridostigmine (Regonol)
Indirect-acting cholinergic drugs:
(Acetyl)cholinesterase inhibitors
MOA
- These drugs produce reversible inhibition of AChE (which destroys Ach)
- by formation of a carbamyl-ester complex which dissociates slowly,
- hence provides longer action of Ach.
- They act preferentially at the neuromuscular junction (NMJ) and
- restore skeletal muscle strength by increasing the availability of acetylcholine.
Indirect-acting cholinergic drugs:
(Acetyl)cholinesterase inhibitors
Used to treat what?
Myasthenia gravis and
Nondepol Neuromuscular Blockade Reversal
Indirect-acting cholinergic drugs:
(Acetyl)cholinesterase inhibitors
ADRs
•nausea,
diarrhea, and
excessive salivation.
Caution in patients with asthma.
If muscarinic effects of such therapy are prominent, they can be controlled by the administration of atropine.
What is the Emergency Issue with Indirect-acting cholinergic drugs: (Acetyl)cholinesterase inhibitors
Note that there is a short amount of time between the occurrence of ADRs and Toxicity- emergency treatment needed if you see fasciculations of voluntary muscles.
Indirect-acting cholinergic drugs:
Central (acetyl)cholinesterase inhibitor
Name one drug:
•Donepezil (Aricept)
Indirect-acting cholinergic drugs:
Central (acetyl)cholinesterase inhibitor
MOA
•inhibits breakdown of AChE; thus causing an increase in Ach
(Donepezil (Aricept))
Indirect-acting cholinergic drugs:
Central (acetyl)cholinesterase inhibitor
What is it used for?
Treatment of mild to moderate Alzheimer’s disease.
Among those who benefit, improvements are seen in quality of life and cognitive functions (eg, memory, thought, reasoning).
There is no evidence the drug leads to substantial functional improvement or prevents progression of Alzheimer’s.
Indirect-acting cholinergic drugs:
Central (acetyl)cholinesterase inhibitor
ADRs
Most ADRs are related to increased cholinergic (muscarinic) effects including GI effects such as nausea and diarrhea, increases gastric acid secretion (monitor for occult bleeding), syncope, bradycardia (thus should be taken at bedtime)
Why are Indirect-acting cholinergic drugs:
Central (acetyl)cholinesterase inhibitor
effective with alzheimer’s patients?
Patients with Alzheimer disease (AD) have reduced cerebral production of choline acetyl transferase, which leads to a decrease in acetylcholine synthesis and impaired cortical cholinergic function.
What is an advantage of donepazil over other drugs?
Donepazil has an advantage over other drugs such as tacrine (another centrally active AchE inhibitor that was the first drug to show success treating AD) because of once-a day dosing (improved adherence), lower side effect profile, and does not require liver function tests for hepatoxicity.
What are anticholinergic drugs also known as?
cholinergic blockers,
muscarinic antagonists
How do anticholinergic drugs work?
MOA: Block Ach at muscarinic receptors
Prototype: atropine
Why is an anticholinergic drug used for eyes?
To get mydriasis
Why is an anticholinergic drug used for CV system?
- Blocks vagal impulses to heart
- Reverses sinus brady (increases HR)
Why is an anticholinergic drug used for the respiratory system?
- Bronchodilation
- SuprprSuppressratory secretions pre-op
Why is an anticholinergic drug used for GI system?
Decreases secretions and tone.
Why is an anticholinergic drug used for the GU system?
to treat bladder spasms
Why is an anticholinergic drug used for the CNS?
- Treat tremors/rigidity of Parkinsonism
- Treat EPS from psychotropic medications
- Sedation
- Motion Sickness
Discuss general ADRs of anticholinergics:
- Photophobia
- Increased Intraocular Pressure
- Dry Mouth
- Constipation
- Urinary retention
- Drowsiness
- Central Anticholinergic Syndrome/ Anticholinergic toxicity (antidote is physostigmine salicylate- increases Ach)
Atropine and Scopolamine
Why administered prior to surgery?
Atropine or scopolamine is administered prior to induction of anesthesia to protect heart from vagal reflexes and prevent excessive salivary & respiratory secretions.
Pts. w/ glucome requires special consideration
What effects on the heart does Atropine have?
•Atropine is used to reverse severe sinus bradycardia in adults and neonates, especially when due to parasympathetic influence (e.g., digoxin, beta blockers).
What effects does atropine have on biliary and ureteral smooth muscle?
•Atropine decreases the tone of the smooth muscle of the biliary tract & ureter and produce relaxation.
What is best use of scopolamine for motions sickness?
Motion Sickness Prevention: Protection is greatest if the scopolamine is applied as a patch [Transderm-Scop] behind the ear at least four hours before the noxious stimulus.
How does Ipratropium (Atrovent) work?
Anticholinergic drugs can relax bronchial smooth muscles by blocking the constrictor effects of the vagus nerve.
The anticholinergic drugs are more effective bronchodilators when administered by aerosol inhalation
What caution should one know about regarding systemic anticholinergics and asthmatic patients?
In spite of their bronchodilatory effect, systemic anticholinergics should be used cautiously in asthmatic patients because of drying of secretions and increased risk of mucus plugs.
What class of drug is recommended as first-line drug for treatment of COPD?
Anticholinergics are recommended as a first line drug be used in treating COPD
Anticholinergic drug:
Oxybutynin (Ditropan XL)
•is the prototype of overactive bladder drugs.
Oxybutynin is both an antimuscarinic and an antispasmodic.
It easily crosses the blood-brain barrier, thus has a higher rate of CNS adverse effects.
inform the patient that adverse effects include xerostomia (70%) constipation, urinary retention, and blurred vision.
Alcohol may enhance the drowsiness
Tolterodine (Detrol)
Anticholinergic drug - •commonly advertised drug for overactive bladder.
Issues with treating overactive bladder in the elderly with anticholinergic drugs:
Anticholinergic adverse effects (dry mouth, blurred vision, constipation, cognitive dysfunction).
This is challenging because the population with the highest prevalence of overactive bladder is the elderly:
patients predisposed to cognitive dysfunction, urinary retention and visual disturbances.
Benzotropine
(Anticholinergic drug)
- Parkinson’s Disease & extrapyramidal symptoms of antipsychotics.
- Parkinsonian tremor and rigidity seem to result from a relative excess of cholinergic activity in the basal ganglia system.
- The tremor of Parkinson’s disease is reduced by centrally acting antimuscarinic drugs
- (e.g., benztropine [Cogentin]; trihexyphenidyl [Artane]).
Diphenhydramie (Benadryl)
Anticholinergic agent
Is often recommended to alleviate extrapyramidal symptoms (EPS) associated with conventional antipsychotic agents.
Types of Somatic NS Drugs
Nondepolarizing Agents
Tubocurarine is the prototype drug but is no longer available in the US
Depolarizing Agents
Succinylcholine [Anectine] (two acetylcholine molecules attached) is the only agent.
Classifying Somatic and Autonomic NS Drug Effects
Sympathetic (adrenergic, Anticholinergic) effect:
- Adrenergic Agonists
- (Alpha 2 Adrenergic Agonist)**
- Anticholinergics
Stimulation of Alpha2 receptors creates a negative feedback loop and inhibits sympathetic outflow (aka sympatholytic).
Alpha2 Adrenergic Agonists- Sympathetic effects:. Dry mouth, constipation, nausea and gastric upset. Sympatholytic effects (similar to parasympathetic): Bradycardia, hypotension, and impotence
To be clear, an anticholinergic drug is NOT an adrenergic agonist (their pre-ganglionic mechanism of action and post-ganglionic transmitters vary).
But their EFFECT is similar and that might help for you to remember their uses and side effects.
Classifying Somatic and Autonomic NS Drug Effects
Parasympathetic (cholinergic, Muscarinic) effect:
- Cholinergic Agonists
- (Alpha 2 Adrenergic Agonist)**
- Alpha Adrenergic Antagonists
- Beta Adrenergic Antagonists
- Anticholinesterase (AChE) inhibitors
