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I used the lecture notes, videos, and textbook from HPRS 2300 Fall 2020 to complete this padlet.

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Alpha-1 Adrenergic Agonists

Alpha 1 is stimulated

Adrenergic Agonists

Stimulates all alpha and beta receptors

Alpha-1 Adrenergic Blocker

Binds to alpha receptors and blocks them

Beta-1 Adrenergic Agonist

Low dose: Stimulates D1 receptors in the kidneys causing vasodilation, increased blood flow

Mod. dose: Stimulates B1  - increases force of contraction and cardiac output

High dose: stimulates A1 receptors causing vasoconstriction and consequently an increase in blood pressure

Beta-2 Adrenergic Agonist

Stimulates B₂ receptors

Beta Blocker

Selective: B1 receptor is blocked

Nonselective: B₁ and B2 receptors are blocked

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Alpha 1:

Locations: glands, smooth muscles, eyes, and most arteries and veins

Alpha 2:

Negative feedback loop of alpha 1

Beta 1:

Located in the heart

Beta 2:

Located on smooth muscle, lungs, uterus, skeletal muscle blood arteries, and coronary arteries

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Released from the adrenal medulla

Acts on adrenergic receptors

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Released at postganglionic nerve ending

Released by the adrenal medulla and neurons

Synthesized from dopamine

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Alpha-1 Adrenergic Agonists

Ex/ phenylephrine (Neo-Synephrine®)

Adrenergic Agonists

Ex/ epinephrine (Adrenalin®)

Alpha-1 Adrenergic Blocker

Ex/ terazosin (Hytrin®)

Beta-1 Adrenergic Agonist

Ex/ dobutamine

Beta-2 Adrenergic Agonist

Ex/ terbutaline (Brethine®)

Beta Blocker

Nonselective ex/ nadolol (Corgard®)

Selective ex/ atenolol (Tenormin®)

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Alpha 1

Organs effected: most arteries and veins, eyes

EPI/ NE Response: vasoconstriction and contraction resulting in pupillary dilation

Alpha 2

Organs effected: Adrenergic nerve ending

EPI/ NE Response: Decrease release of NE

Beta 1

Organs effected: Heart

EPI Response: Increase in heart rate, increase in force of contraction, and increase in atrioventricular conduction

NE Response: Increase in heart rate, increase in force of contraction, and increase in atrioventricular conduction (not as much of an increase as EPI)

Beta 2

Organs effected: bronchodilator smooth muscle, uterus, coronary and skeletal blood vessels

EPI Response: Bronchodilation, relaxation, and vasodilation

NE Response: Norepinephrine does not stimulate B2 responses

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muscarinic

decrease heart rate, bronchoconstriction, increase digestion, increase GI secretions, and increase urination, and pupillary constriction

nicotinic 1 (Nn)

nicotinic 2 (Nm)

If stimulated, muscle contracts

ALL are stimulated by ACH

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Precursor to NE

Stimulates alpha, beta, and dopaminergic receptors

Produced by the hypothalamus

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Acetylcholine (ACH) -

Released at the ganglia from presynaptic nerve endings

Produced by cholinergic neurons

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Also known as the cholinergic system, the Parasympathetic division is responsible for the "rest and digest" responses

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Also known as the adrenergic system, the Sympathetic division of the ANS is responsible for the "Fight, Flight, or Fright" responses

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Direct - Acting Cholinergic Agonists

stimulates muscarinic receptors

mimics ACH

Indirect - Acting Cholinergic Agonists

inhibits acetylcholinesterase which destroys ACH  at the synapse

increases ACH present

Anticholinergic

binds to the cholinergic receptor and blocks

competitive antagonism

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muscarinic

Located on the cardiac, smooth muscle and glands

nicotinic 1 (Nn)

Located at the ganglia of parasympathetic nerves and sympathetic nerves (synapse)

nicotinic 2 (Nm)

Located at the somatic, neuromuscular junction of skeletal muscle

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Direct – Acting Cholinergic Agonists

Ex/ Pilocarpine (Pilocar®)

Indirect – Acting Cholinergic Agents

Ex/ Neostigmine (Prostigmin®)

Anticholinergic

Ex/ Dicyclomine (Bentyl®)