Cholinergics

Front 1

Acetylcholine

Back 1

Class: ANS NT
Mechanism: ACh is the “workhorse” of the ANS. The NT of all preganglionic neurons (N) as well as the NMJ (N), adrenal medulla (N), sweat glands (M), and postganglionic PSNS neurons (M). The vasculature also has receptors (M) although these are NOT innervated, therefore there is no endogenous ACh released (keep in mind with cholinergic drugs though)
Clinical Effects: Worthless as a drug: (Terrible absorption [polar], Rapid degradation [AChE], No specificity [nicotinic v. muscarinic]
Contra/Side Effects: All over the map (if it could even get to the receptors)

Notable toxins:
-black widow: lipase destroys cholinergic ends
-other venom: block AChRs
-botulin: blocks influx of Ca2+
Notes: N= nicotinic
M= muscarinic

Front 2

Muscarine
Bethanachol
Methacholamine

Back 2

Class: ACh Agonist
MOA: Muscarine is a toxin from a mushroom. Muscarinic receptors (4.4 A) are what ACh bind.

Activates postganglionic PSNS response (“rest & digest”), sweat glands (Sympathetic), and causes NO mediated vasodilation when administered (no innervation)

B – ACh + beta CH3 + terminal amino
M – ACh + beta CH3
Clinical Effects: B – Post GI operation to recover peristalsis
M – No longer used (classic anti-hypertensive)

Contra/Side Effects:
Notes:

Front 3

Nicotine

Back 3

Class: Ach Agonist
MOA: Nicotine is a toxin from cigarettes.
Nicotinic receptors (5.9A) are what ACh bind.

Activates preganglionic PSNS & SNS (NN : non-specific, depends on which system predominates), NMJ (NM : contraction), and adrenal medulla (NN : Epi / NE release)
Clinical Effects: None (non-specific)

Noted to increase memory, attention, and relaxation

Contra/Side Effects: Highly addictive
Increases in HR and BP (due to Epi release) + Sympathetic effects in general

Notes:

Front 4

Carbachol

Back 4

Class: Muscarinic / Nicotinic Agonist
MOA: ACh + terminal amino
Acts at muscarinic receptors (CV, PSNS) at low doses, nicotinic receptors at high doses (ganglia, adrenal medulla, NMJ)

Clinical Effects: Local application used in treatment of glaucoma (opens canal of Schlemm = dec. IOP)
Contra/Side Effects:
Notes:

Front 5

Atropine

Back 5

Class:Muscarinic Antagonist
MOA: Tertiary amino, readily absorbed
Clinical Effects: Corrects bradycardia
(Local: Ophtho: Refraction)
Contra/Side Effects: Contra: Narrow angle glaucoma
Notes:

Front 6

D-Tubocurare
(Pancuronium)

Back 6

Class: Nicotinic (NM) Antagonist (10C)
MOA: NMJ blocking agent (decreases size of EPP = decreased probability of AP)
Clinical Effects: Induce flaccid muscle paralysis in surgery (South American poison darts)
Contra/Side Effects:
Notes:

Front 7

Hexamethonium
Trimethaphan

Back 7

Class: Nicotinic (NN) Antagonist (6C)
MOA: Non-specific ganglionic blockade
Clinical Effects: No longer used.

Classically used for acute hypertensive crisis (see side effects)
Contra/Side Effects: Predominant system blocked (i.e. SNS – vasculature + sweat glands / PSNS – everything else)
Notes: