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"fight or flight"

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acetylcholine(ACH)

norepinephrine(NE)

epinephrine(EPI)

dopamine(DA)

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"rest and digest"

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acetylcholine(ACH)

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muscarinic- located on glands, smooth muscle, and cardiac muscle

nicotinic 1 (Nn)- located on the ganglia of parasympathetic nerves and synapses

nicotinic 2 (Nm)- located on neuromuscular junction of skeletal muscle

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Heart- Decreases heart rate, AV conduction, and a slight decrease in contractility.
Intestines/Digestive Tract- Increases motility and secretions.

Pupil: Constriction (miosis)

Respiratory passages- Bronchoconstriction which lowers the passage

Urinary Bladder- Contracts

Sphincter- Relaxes

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alpha 1- located on glands, smooth muscles, eyes, arteries, and veins

alpha 2- located on nerve endings(response to alpha-1)

beta 1- located on the heart

beta 2- located on smooth muscles, lungs, uterus, skeletal, and coronary arteries

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Direct Acting Cholinergic Agonist-
Mimics ACH by binding to muscarinic receptors in the body.

Indirect Acting Cholinergic Agents-
Inhibits acetylcholinesterase which is the enzyme that destroys ACH which will increase the ACH in the body.

Anticholinergics- Binds to cholinergic receptors creating competitive antagonism in the body.

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Adrenal medulla- Releases epinephrine.

Arteries- Vasoconstriction of most except coronary and skeletal arteries.

Heart- Increases heart rate, AV conduction, and increases contractility.

Intestines: Decreases GI motility and secretions.

Pupil- Dilates (mydriasis).

Respiratory passages- Bronchodilation, opens up airway to breath.

Urinary Bladder- Relaxes.

Sphincter- Contracts.

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

Indirect Acting Cholinergic Agents:
neostigmine (Prostigmin®)

Anticholinergics:
atropine
dicyclomine (Bentyl®)

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Alpha-1 Adrenergic Agonists: Stimulates alpha-1 receptors which causes the contraction of smooth muscle, increases blood pressure, vasoconstriction, and a decongestant effect.

Adrenergic Agonists: Stimulates alpha and beta receptors which causes vasoconstriction, increases blood pressure, stimulates the heart, and a bronchodilator.

Alpha-1 Adrenergic Blockers: Binds to alpha-1 receptors and blocks them which causes smooth muscle to relax, decrease blood pressure, and increase urine flow.

Beta-1 Adrenergic Agonists: Stimulates beta-1 receptors which depending on the dose effects the body. Low doses will effect the kidneys and cause increased renal blood flow, and vasodilation. Moderate doses will effect the heart and increase the force of contraction which increases the cardiac output.

Beta-2 Adrenergic Agonists: Stimulates beta-2 receptors which causes bronchodilation and relaxes the uterus.

Beta Blockers (Nonselective and selective): Selective blockers will block beta-1 receptors which will decrease cardiac output, decrease heart rate, decrease force of contraction, decrease conduction, and decrease blood pressure. Nonselective blockers block beta-1 and beta-2 receptors which will decrease cardiac output, decrease blood pressure, decrease force of contraction, decrease heart rate, decrease conduction, and cause bronchoconstriction.

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

Adrenergic Agonists:
epinephrine (Adrenalin®)

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

Beta-1 Adrenergic Agonists:
dobutamine

Beta- 2 Adrenergic Agonists:
formoterol (Foradil®)
albuterol (Proventil®, Ventolin®)

terbutaline (Brethine®)

Beta Blockers:
-Nonselective
nadolol (Corgard®)

propranolol (Inderal®)

timolol (Blocadren®)
-Selective
atenolol (Tenormin®)

metoprolol (Lopressor®)