Autonomic Pharmacology

Nervous system overview

-NS= CNS + PNS

-CNS: brain + spinal cord

-PNS: Somatic NS and ANS

-ANS: SNS and PSNS

ANS divisions

-PSNS/SNS can control same organs but opposite effects

-PSNS: rest and digest (relax/conserve)

-SNS: fight and flight (mobilize)

rest/digest vs fight/flight

*anti-chol drugs block these things!

PSNS vs SNS (w/ hand analogy)

Hand Analogy: top/bottom=PSNS, middle=SNS

-Left hand thumb/pinky: PARASYMPATHETIC cranial and sacral

-Right hand fist: SYMPATHETIC thoracic and lumbar

-Left long fingers: long preganglionic

-Right fist short fingers: short preganglionic

-Left: two fingers are independent of each other – discrete

-Right fist: all work together – massive response

-Left Hawaiian hand sign: cool alright (para) conserve

-Right fist: flight/fight

ANS controls…

-ANS controls involuntary bodily functions

-Organs affected – heart, lung, GI, etc

ANS receptors

*Pre: Ach effects SNS and PSNS

*Post: SNS=NE; PSNS=Ach

*nicotionic=all; muscarinic=just PSNS

^so if drug effects Ach it effects all 3; if just NE effects 1 place

ANS receptor subtypes (list)

SNS summary

-Preganglionic neurons= thoracolumbar

-Energy expenditure

-“Fight or Flight”

-Drugs

• Sympathomimetic

• Sympatholytic

PSNS summary

-Preganglionic neurons= craniosacral

-Energy conservation

-“Rest and Digest”

-Drugs:

• Parasympathomimetic

• Parasympatholytic

Knowledge check

-2 ANS Divisions

-Describe SNS

-Describe PSNS

-NT Preganglionic SNS/PSNS

-NT Postganglionic  SNS/PSNS

-Pre/Post- gang - Receptors – SNS

-Pre/Post- gang - Receptors – PSNS

-SNS, PSNS

-Fight/flight

-Rest and digest

-Ach

-SNS NE; PSNS Ach

-Pre-nicotinic, post-adgrenergic alpha beta

-pre-nicotinic, post cholinergic muscarinic

*all nicotinic= “whole gang smokes”

Adrenergic Drugs

-NT

-Actions

-Drugs can

-Use

-Neurotransmitters: Norepinephrine, Epinephrine

-Actions: Agonist, Antagonist

Drugs can

-Facilitate norepinephrine and epinephrine release or

-Activate/block the adrenergic receptors

Use

-Reduce bleeding by constricting arterioles

-Slow diffusion of local anesthetics

-Decongest mucous membranes

-Raise blood pressure when patient is in shock or hypotensive

location sympathetic/adrenergic receptors

α₁

-Prostate gland

-Arterial smooth muscle

α₂

-Pre-synaptic autoreceptors on sympathetic nerves

-Brainstem

β₁

-Heart

-Kidneys – (Renin release)

β₂

-Lungs

-Liver

-Arterial smooth muscle

alpha 1 adrenergic: agonist

-vasoconstriction (ex=eyedrops for bloodshot eyes)

alpha 1 adrenergic: antaognist

-vasodilation

-relaxation of prostatic

alpha 2 adrenergic: agonsist

-Reduced release of NE

-treat HTN

alpha 2 adrenergic: antagonist

-increased release of NE

-NO clinical uses! (*phentolamine not on quiz, only one use for it)

beta 1 adrenergic: agonist

-in heart

-increase HR

-used for heart failure (will die if don’t take)

beta 1 adrenergic: antagonist

-lowers HR (so can’t use HR to reflect activity tolerance)

-meds all end in “lol”

-reduced cardiac output

beta 2 adnregeric: antagonist

-better than PSNS antagonist

-glucose mobilization, relaxation of bronchial (breathe better)

-asthama, COPD

-increases HR (bc effects beta 1 as well)

-Albuterol inhaler

beta 2 adrenergic: antagonist

-for ED only!

importance of selectivity: non-selective beta blockers VS cardioselective beta blockers

Non-selective Beta-Blockers: Beta 1 and 2

-Decrease CO in the heart, also binds to receptors in lungs & liver

-Ex. propranolol

-Implications?= ED, increases difficulty breathing but if lung or liver problem

Cardioselective Beta-Blockers: ONLY Beta 1 (so no effect on lung!)

-Reduces CO WITHOUT producing effects in lungs or liver

-Ex. metoprolol

-Implications?: just effects cardiac

cholinergic receptor 2 drugs

-Nicotinic

-Muscarinic: 5 different types in 3 places (CNS, Heart, Smooth muscle)

Muscarinic Agonists: Parasympathomimetic  

*eye problem/increase eye pressure

*bowel movements and motility

*overactive bladder/relaxes bladder so allows to fill

Cholinergic Application questions: agonist or antagonist

-if at dentist and goal is decreased salivation

-if COPD and want open airway

-agonist

-antagonist (SNS ag and PSNS antag)

Muscarinic Direct Acting Drugs Agonist

-Glaucoma: Increase intraocular pressure

• Goal: Decrease intraocular pressure

• Drug: Pilocarpine –  increases flow of aqueous humour > decreasing pressure

-Urinary retention

• Goal: Increase urination

• Drug: Bethanechol – contract detrusor muscle for increase urination

Muscarinic Indirect Acting - Anticholinesterases

-Inhibits acetylcholinesterase to prevent acetylcholine metabolism (prolongs action of ACh)

-Examples

• Edrophonium – Myasthenia Gravis - autoimmune disease – mm weakness unable to maintain a contraction, drug allows ACh to remain longer in junction allowing mm contraction

*not enough Ach so med increases Ach

Cholinergic Agonist: Adverse Effects

-GI distress (N/V, diarrhea)

-Increased salivation secretions

-Bronchoconstriction

-Bradycardia

-Impaired vision

-Increased sweating

Muscarinic Antagonists (Anti-Muscarinic) 

*opposite antagonist and for dif reasons/diseases

Cholinergic Antagonists: Side Effects

-Dry mouth

-Blurred vision

-Urinary retention

-Constipation

-Tachycardia

-Agitation