Ganglionic Stimulant

- Acts @ neuronal nicotinic rec in autonomic ganglia

- Effects depend on pre-existing dominance of symp vs parasymp systems in effector tissues

Nicotine

(most addictive drug ever)

Stimulant at low doses (nicotonic agonist)

-normal depolarization of cell membrane surrounding nicotinic receptors

Depressant at high doses (nicotinic antagonist)

-persistent depolarization and desensitization of nicotinic receptors

in all organs where Ach is transmitter

ALL SUBTYPES

-CNS (hypothalamus, medullary centers, chemoreceptor zones to wean off addiction)

-CV, GI (via ANS)

-Skeletal Muscle (muscular subtype nicotinic rec in neuromusc junctions)

-Most likely site of addiction

 - Initial effect of nicotine is on CNS (inc respiration)

-can cause vomiting by stimulating CTZ (chemoreceptor trigger zone)

-Higher doses --> CNS stimulation to depression

CVS (Autonomic)

[Cardiovascular System]

-Complex

-low doses stimulate autonomic ganglia, increases periph vasoconstriction -> acute hypertension

-high doses may dec bp, most likely due to reversal of ganglionic stimulating action to a ganglionic blocking action

-Nicotine inc motility at low doses, dec at high doses

-first smoke will make you poop

-Nicotine is rapid acting, absorbed from ALL routes

-metabolized mostly in liver, excreted by kidney as cotinine

-passes placental and blood brain barrier (BBB)

Symptoms change (inc saliva, nausea, vomiting, diarrhea to fainting, drop in bp, prostration, collapse)

-Treatment is symptom directed

1. atropine for GI symptoms

2. adrenergic agonists if too high

- half life of 2 hours so just wait it out

-used to wean people off smoking (must be high dose)

-toxic after accidental ingestion by kids, treat: induce vomiting and charcoal tablets

-green tobacco sickness from skin exposure in the fields