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- Book: Pharmacology for Health Professionals, 4th special edition
- Powerpoint

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Another name for the parasympathetic Nervous system is Cholinergic

We use this system in rest and digest

Neurontransmitters

NT released at ganglia is ACH (cholinergic)

NT released at postganglionic nerve endings is ACH (cholinergic)

Muscarinic:

located on cardiac, smooth muscle, and glands

at parasympathetic postganglionic nerve endings

decrease HR, bronchoconstriction, ↑ digestion, ↑ GI secretions, and ↑ urination, pupillary constriction

Nicotinic 1 (Nn):

at ganglia of parasympathetic nerves and sympathetic nerves (synapse area)

Nicotinic 2 (Nm):

somatic, neuromuscular junction of skeletal muscle

If stimulated, muscle contracts.

(ALL are stimulated by ACH)

Parasympathetic Effect on organs

Arteries = most not supplied by parasympathetic nerves

Heart = Decrease heart rate and SV conduction, slightly decrease in contractility

Intestines, GI movement & secretions = increased

Postganglionic neurotransmitter = Acetycholine rebased

Pupil of the eye = Miosis (constriction of the pupil)

Lower respiratory passage = bronchoconstriction

Urinary bladder = contraction

Urinary sphincter = relaxation

Drug Classifications & Drugs for the Parasympathetic Nervous System

Cholinergics/Parasympathomimetics:

stimulates muscarinic receptors of bladder and GI tract to prevent constipation and urinary retention post-op and in the elderly

Drugs

pilocarpine (Pilocar®)

bethanechol (Urecholine®)

Cholinergics/Parasympathomimetics

inhibit acetylcholinesterase, the enzyme that destroys ACH in the synapse, increases ACH

Drugs

neostigmine (Prostigmin®)

Anticholinergics/Parasympatholytics

bind to a cholinergic receptor

acts as a blocking drug; competitive antagonism

Drugs

atropine

dicyclomine (Bentyl®)

ipratropium bromide (Atrovent®)

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Another name for the Sympathetic Nervous system is Adrenergic

We use this system in Fight, Fright or Flight situations.

Neurontransmitters

Acetylcholine (ACH)

Released at ganglia from presynaptic nerve endings

Norepinephrine (NE)

Released at postganglionic nerve endings

Manufactured from dopamine

Released by adrenal medulla and neurons

Epinephrine (EPI)

Acts on adrenergic receptors

Produced by adrenal medulla

Dopamine (DA)

Precursor to NE

Stimulates many receptors (alpha, beta, dopaminergic); different actions in the body from DA all depends on the dose that has been administered

Sympathetic Effect on organs

Adrenal Medulla = Release of Epinephrine

Arteries = Vasoconstriction (Coronary arteries & arteries to skeletal muscle do not vasoconstrict, they dilate )

Heart = Increase heart rate & AV conduction. Increase contractility

Intestine, GI movement and secretions = Decreased

Postganglionic neurontransmitter = Norephiphrine released

Pupil of the eye = Mydriasis (Dilations of the pupil)

Lower respiratory passages = Bronchodilation

Urinary Bladder = relaxation

Urinary Sphincter = contraction

Drug Classifications for the Sympathetic Nervous System

Alpha-1 receptor =  EPI & NE effect (vasoconstriction, pupillary dilation)

Alpha-2 receptor = EPI & NE effect ( decrease release of NE )

Beta-1 receptor = EPI effect (greater increase in heart rate, force of contraction &                       AV conduction ) NE effect = (medium increase in heart rate, force of contraction &                     AV conduction

Beta-2 receptor = EPI effect (Bronchodilation, relaxation,vasodilation)                                                NE effect (NE not stimulated)

Medications for the Sympathetic Nervous System

Alpha-1 Adrenergic Agonists:

alpha-1 receptor is stimulated

contraction of smooth muscle, blood vessels constrict, increases BP

vasoconstriction of nasal passages  decongestant effect

Drugs

Ephedrine (Adrenalin®)

Phenylephrine (Neo-Synephrine®)

Adrenergic Agonists:

Stimulates all alpha and beta receptors, an exception

Vasopressor-vasoconstriction, increases BP

Cardiac stimulant

Bronchodilator

Drugs

epinephrine (Adrenalin®)

Alpha-1 Adrenergic Blocking Drugs:

binds to alpha-1 receptors and blocks them

relaxation of smooth muscle

vasodilation of blood vessels, decreases BP

relaxes smooth muscle of ureters and increases urine flow

Drugs

prazosin (Minipress®)

terazosin (Hytrin®)

doxazosin (Cardura®)

Beta Adrenergic Agonists

Low dose-stimulates dopaminergic (d-1) receptors in kidneys causing vasodilation and increased renal blood flow

Moderate dose-stimulates  beta 1 receptors-heart, increases force of contraction and cardiac output

High dose- stimulates alpha-1 receptors causing vasoconstriction  increase in blood pressure

Drugs

dobutamine

Beta Adrenergic Agonists

stimulates beta 2 receptors

relaxation of the smooth muscle of the lungs  bronchodilation

relaxation of the smooth muscle of the uterus

Drugs

albuterol (Proventil®, Ventolin®

terbutaline (Brethine®)

formoterol (Foradil®)

salmeterol (Serevent®)

Beta-Adrenergic Blocking Drugs

beta-1 receptor is blocked (antagonizes beta-1 effects of NE and EPI)

decreases force of contraction  (negative inotropic), decreases cardiac output

decreases HR  (negative chronotropic)

decreases conduction (negative dromotropic)

decrease in cardiac output also decreases BP

Drugs

atenolol (Tenormin®)

metoprolol (Lopressor®)

Beta-Adrenergic Blocking Drugs

block beta-1 and beta-2 receptors

decreases force of contraction  (negative inotropic), decreases cardiac output

decreases HR  (negative chronotropic)

decreases conduction (negative dromotropic)

decrease in cardiac output also decreases BP

can cause bronchoconstriction

Drugs

nadolol (Corgard®)

propanolol (Inderal®)

timolol (Blocadren®)