ANS Flashcards
How do muscarinic receptors act
they are G-protein coupled receptors
How to nicotinic receptors act
They are ion-channel mediated (increase Na+ movement into cells)
Types of nicotinic receptors
NM and NN
Effects of M2 receptors
Heart: reduce HR, FOC and CO
Effects of M3 receptors
- blood vessel: vasodilation and and decrease BP 2. smooth muscle: contraction–> broncospasm, diarrhea, urination 3. Pupil: miosis 4. Glands: increase salivation (increase lacrimation), sweating, gastric acid
M1 receptor type
Gq
Effector enzyme at Gq
Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.
Effector enzyme at M1
Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.
M3 receptor type
Gq
Effector enzyme at alpha 1
Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.
Effector enzyme at M3
Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.
alpha 2 receptor type
Gi
Gq second messenger
stimulates PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.
alpha 1 receptor type
Gq
beta 1 effector enzyme
Gs–>stimulate adenylyl cyclase–>increase cAMP
M2 receptor type
Gi
Gi effector enzyme
Gi–>inhibit adenylyl cyclase–>decrease cAMP
alpha 2 effector enzyme
Gi–>inhibit adenylyl cyclase–>decrease cAMP
Receptors that act via Gs
beta 1, beta 2, beta 3
M2 effector enzyme
Gi–>inhibit adenylyl cyclase–>decrease cAMP
beta 2 effector enzyme
Gs–>stimulate adenylyl cyclase–>increase cAMP
Receptors that act via Gq
M1, M3 & alpha 1
beta 1 receptor type
Gs
beta 2 receptor type
Gs
beta 3 receptor type
Gs
M1: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gq 2. Stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3. Neurons 4. CNS effects
Receptors that act via Gi
alpha 2, M2
Effect of tyrosine hydroxylase
converts Tyrosine–>DOPA RATE LIMITING STEP in formation of Dopamine ADRENERGIC TRANSMISSION
NN receptor 1. location 2. type
- ANS ganglia & Adrenal Medulla 2. Na/K channel
alpha 2 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gi 2. Inhibit adenylyl cyclase–>decrease cAMP 3. presynaptic neurons 4. reduces release of norepinephrine–>bradycardia & hypotension
M3: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gq 2. Stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3/4. Smooth muscle and; glands: –>contraction (except in bv–>vasodilation–>decrease BP); diarrhea, bronchoconstriction, urination, increase secretions, salivation, stomach acid, sweating, lacrimation Pupil and ciliary muscle: contracts–>miosis; increase flow of aqueous humor
alpha 1 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gq 2. Stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3/4. blood vessels–> vasoconstriction–>increase BP pupil (iris)–>dilation (mydriasis) smooth muscle–>sphincter contraction–>constipation & urinary retention
Metyrosine
inhibits tyrosine hydroxylase–>so it can’t convert tyrosine to DOPA AFFECTS ADRENERGIC TRANSMISSION Tyrosine is co-transorted into pre-synaptic nerve terminal with Na+
beta 3 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gs 2. stimulate adenylyl cyclase–>increase cAMP 3. fat tissue 4. Lipolysis
Rate-limiting step for ACh synthesis
choline uptake
M2: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gi 2. Inhibit adenylyl cyclase–>decrease cAMP 3. Heart 4. reduces HR, FOC and CO
Receptor in adrenal medulla & response
NN–>secretion of Epi & NE
beta 3 effector enzyme
Gs–>stimulate adenylyl cyclase–>increase cAMP
Where you find NN
Adrenal medulla & autonomic ganglia
beta 2 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gs 2. stimulate adenylyl cyclase–>increase cAMP 3/4. smooth muscles–> relaxation–>bronchodilation, urinary retention, constipation, uterus relaxation liver–> heart–>
beta 1 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects
- Gs 2. stimulate adenylyl cyclase–>increase cAMP 3. heart 4. contraction, increased HR increases renin release & juxtaglomeruluar apparatus
Reserpine
inhibits uptake of dopamine into vesicles (inhibits storage) AFFECTS ADRENERGIC TRANSMISSION
Bretylium
inhibits VAMPs & SNAPs which enable vesicles containing NE/ATP/E to bind to membrane & release–>inhibits release AFFECTS ADRENERGIC TRANSMISSION
Guanethidine
inhibits VAMPs & SNAPs which enable vesicles containing NE/ATP/E to bind to membrane & release–>inhibits release AFFECTS ADRENERGIC TRANSMISSION
cocaine
inhibits reuptake of messengers (NE/E/Dopamine) AFFECTS ADRENERGIC TRANSMISSION
Tricyclic antidepressants
inhibits reuptake of messengers (NE/E/Dopamine) AFFECTS ADRENERGIC TRANSMISSION
Where does NE work
at presynaptic alpha 2 (autoreceptors) & at postsynaptic alpha 1 receptors
Hemicholinium
AFFECTS CHOLINERGIC TRANSMISSION inhibits uptake of Choline into presynaptic nerve terminal (co-transorter with Na+); RATE-LIMITING STEP
Vesamicol
AFFECTS CHOLINERGIC TRANSMISSION inhibits storage of ACh in the presynaptic nerve terminal (ACh can’t be properly taken up & stored in vesicles)
Botulinum
AFFECTS CHOLINERGIC TRANSMISSION inhibits release of ACh (vesicles can’t properly dock & release)
rate limiting step for catecholamine synthesis
tyrosine hydroxylase
Cholinergic neurotransmission is terminated by
AChE
Adrenergic neurotransmission is terminated by
reuptake
DAG function
modulates action of protein kinase C
Myasthenia Gravis Symptoms; Dx; what makes it worse?
autoimmune disorder that involves antibody mediated disruption of NMJ receptors Production of antibodies that decreases the number of functional nicotinic receptors on the muscle end plates Sx: transient weakness with ptosis, diplopia, difficulty speaking, swallowing & extremity weakness. Severe disease may affect all muscles including those used in respiration infection and thyroid dysfunction worsen the symptoms Dx = blood ACh receptor antibody level
result of IP3
IP3–>Ca2+ release from intracellular storage–>smooth muscle contraction
Somatic nervous system receptors & are they cholinergic or adrenergic
NM–>cholinergic
Cholinergic nerves
- all nerve fibers in somatic nervous system = NM 2. All PRE-ganglionic fibers in ANS (SYMPATHETIC & PARASYMPATHETIC) = NN 3. All POSTganglionic fibers in PARAsympathetic nervous system = M1-3
Effect of acetylcholine
DUMBBELSS: D=diarrhea (Smooth muscle contraction & sphincter relax) U=urination (Smooth muscle contraction & sphincter relax) M=miosis (pupil & ciliary muscle contraction*) B=bradycardia (reduce HR, FOC, CO & vasodilation reduces BP) B=bronchoconstriction (Smooth muscle contraction) E=excitation of skeletal muscle L=lacrimation S=secretion S=sweating Sphincters: relaxation smooth muscle contraction EXCEPT in bv->VASODILATION *use for near vision
M3 location & effects
- smooth muscles (GIT, Bronchial, detrussor): contraction–>diarrhea, bronchoconstriction & urination. EXCEPT BV–>vasodilation–>decrease BP due to release of NO 2. Glands–> increase salivation, lacrimation, sweating, gastric acid 3. Pupil–> Miosis–>increase outflow of aqueous humor–>decrease IOP 4. Ciliary Muscle–>contraction 5. Trigone & sphincters–>relaxation–>urination
Indirect Cholinergic Agonists
act by inhibiting metabolism of ACh–>increases concentration in synapse–>increases action of ACh
Direct Cholinergic agonists examples
- Acetylcholine (B) 2. Bethanechol (M) 3. Pilocarpine (naturally occurring alkaloid; M) 4. Carbachol (like bethanechol, M&N) 5. Methcholine 6. Nicotine (like pilocarpine, N) Direct cholinergic agonists = bind directly to cholinergic receptors
Indirect Cholinergic Agonist Examples
- Neostigmine (B) 2. Physostigmine (B) 3. Pyridostigmine (B) 4. Edrophonium (B) 5. Tacrine, Donepezil (B) 6. Ecothiophate (B) 7. Malathion, Parathion, Sarin (B) 1-5 are used to treat Myasthenia Gravis, Alzheimers & Glaucoma
Woman with: -dry skin. -tiredness and fatigue – which are common and can lead to total exhaustion. -muscle pain. -joint pain, stiffness and swelling. -vasculitis (inflammation of blood vessels)
Sjorgens syndrome
Acetylcholine
- Direct Cholinergic Agonist 2. both Muscarinic & nicotinic actions 3. bc of non-specific actions & rapid inactivation by acetylcholinesterase, this drug has no clinical use 4. Vasodilation by ACh is due to the release of EDRF (endothelium derived relaxing factor, aka NO)
Bethanechol DOA; Uses; MOA
- Direct Cholinergic Agonist 2. strong muscarinic action & little or no nicotinic action 3. orally active, poor lipid solubility 4. DOA = 30m-2h Therapeutic uses: 1. paralytic ileus 2. non-obstructive urinary retention (ie post-op) MOA = stimulates M3 receptors–>increase bowel movements & bladder contraction no N effects
DOC for treating paralytic ileus or non-obstructive urinary retention
Bethanechol
Pilocarpine Uses; DOA
- alkaloid 2. Has mucarinic activity only 3. lipid-soluble & penetrates cornea very well 4. DOA = 30m-2h 5. Therapeutic Uses: 1. Glaucoma: due to increased intraocular tension 2. Sjorgens syndrome: chronic, inflammatory autoimmune disorder characterized by dry mouth (xerostomia) & dry eye (keratoconjunctivitis sicca. Works to control these symptoms
Drug used to reduce dry mouth
Pilocarpine
Drug used to treat Sjorgens syndrome
Pilocarpine
Reversible Indirect acting Cholinergic agonists
- Neostigmine 2. Physostigmine 3. Pyridostigmine 4. Edrophonium 5. Tacrine–used to treat alzheimers 6. Donepezil–used to treat alzheimers These are all short-acting & the enzyme is reactivated and hydrolyzes ACh as usual
Irreversible Indirect acting Cholinergic agonists
- Ecothiophate–used to treat glaucoma 2. Malathion 3. Parathion 4. Sarin These are all long-acting; enzyme reactivation takes extremely long time or almost doesn’t take place–>persistent action of ACH in body Ecothiophate is the only one used therapeutically; the rest are insecticides or war gases
Physostigmine: Use; MOA
tertiary amine; lipid soluble–>good eye penetration & CNS penetration; used to treat Glaucoma MOA = reversible inhibition of AChE–> increase ACh Used as a TOPICAL treatment in Glaucoma; Causes miosis–>increases outflow of aqueous humor–>decreases IOP reverses the central & peripheral signs of muscarinic blockade
Neostigmine
quatrenary amine; lipid INSOLUBLE, NOT used to treat Glaucoma
transient weakness with ptosis, diplopia, difficulty speaking, swallowing & extremity weakness
symptoms of myasthenia gravis Dx = blood ACh receptor antibody level
Tx of Myasthenia Gravis
- AChE inhibitors: Neostigmine, pyridostigmine, edrophonium (these are all reversible) 2. immunosuppressants & corticosteroids 3. Thymectomy (bc thyroid dysfunction worsens symptoms)
Neostigmine: use; method given
Reversible AChE Inhibitor used in acute cases of myasthenia gravis; given via IV
Pyridostigmine: use; method given
Reversible AChE Inhibitor; has a longer duration of action than neostigmine, so good for maintenance/long term therapy in myasthenia gravis. 2. Given orally
Edrophonium: use
Reversible AChE Inhibitor; shortest acting for 5 minutes 2. used in diagnosis of M. Gravis & to differentiate myasthenic & cholinergic crisis by doing a Tension test.
Myasthenic Crisis
if drug therapy is inadequate patients develop severe muscle weakness
Cholinergic crisis
if excessive amounts of drugs have been used, patients will become paradoxically weak because of nicotinic depolarizing blockade of motor end plate
Tensilon test
Used to differentiate myasthenia crisis from Cholinergic crisis. small doses of edrophonium (1-2mg IV) will produce NO RELIEF or even WORSEN weakness if the patient is receiving EXCESSIVE AChE Inhibitor therapy = cholinergic crisis patient will improve with edrophonium if has myasthenic crisis–> may be indication for increase in AChE inhibitor dosage
Patient with severe muscle weakness improves with edrophonium given by IV
Patient had myasthenia crisis–> may be indication for increase in AChE inhibitor dosage
Patient with severe muscle weakness has no relief when edrophonium given by IV; may even have worsening of symptoms
patient had cholinergic crisis
Alzheimers Disease
progressive disorder involving neural degeneration in the cortex leading to a marked loss of memory & of the ability to carry on ADL; MCC of degenerative dementia mostly due to loss of cholinergic neurons, thus mainstay of treatment is ACh therapy; Cause unknown Tx: AChE Inhibitors like Tacrine, Rivastigmine & Donepezil
Tx for OP Poisoning
- Atropine: muscarinic receptor blocker (Anticholinergic drug) given via IV large doses until you observe mydriasis, tachycardia, & dryness of mouth Can’t control the nicotinic effects of OP poisoning, just blocks the muscarinic receptor) Also doesn’t have any role in reversing the CNS effects of OP poisoning 2. Pralidoxime (2-PAM): AChE reactivator; acts by hydrolyzing (reactivating) the drug bound enzyme. Should be given as early as possible, before “aging of the enzyme” OP antagonist.
Treatment for Alzheimers
AChE Inhibitors like Tacrine, Rivastigmine & Donepezil
Tacrine
AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)
Rivastigmine
AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)
Donepezil
AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)
fasciculations followed by paralysis
nicotinic toxicity
Miosis, blurred vision, bradycardia, salivation, sweating, urination, bronchial constriction, vomiting, diarrhea
symptoms of organophosphate poisoning; mainly due to stimulation of muscarinic receptors Due to phosphorylation (irreversible inhibition) of the enzyme resulting in excess ACh
3 cardinal signs of atropinization
mydriasis, tachycardia & dry mouth
Pralidoxime (2-PAM)
AChE reactivator; acts by hydrolyzing (reactivating) the drug bound enzyme. Should be given as early as possible, before “aging of the enzyme” OP antagonist.
Atropine
muscarinic receptor blocker (Anticholinergic drug) given via IV large doses to treat OP poisoning until you observe mydriasis, tachycardia, & dryness of mouth Can’t control the nicotinic effects of OP poisoning, just blocks the muscarinic receptor) Also doesn’t have any role in reversing the CNS effects of OP poisoning
Features of toxicity of cholinergic drugs (OP poisoning)
DUMBBELSS D=diarrhea, abdominal cramps, vomiting (Muscarinic) U=urination (Muscarinic) M=miosis (Muscarinic) B=bradycardia (Muscarinic) B=bronchospasm (Muscarinic) E=excitation of skeletal muscle (Nicotinic)* L=lacrimation (Muscarinic) S=salivation (Muscarinic) S=sweating (Muscarinic) *Atropine can’t fix nicotinic symptoms bc just blocks muscarinic receptor
methacholine challenge test
primarily used to diagnose bronchial hyperreactivity = hallmark of asthma & occurs in COPD subject inhales aerosolized methacholine–>bronchoconstriction other therapeutic uses are limited by its adverse cardiovascular effects = bradycardia & hypotension (bc it’s a cholinomimetic)
Use of Edrophonium
diagnosis of M. gravis
Use of neostigmine
Tx of M. gravis acts on cholinesterase; N&M effects
43 yo unable to continue picking vegetables: unsteady gait, difficulty speaking, swallowing, blurry vision, watery eyes, tightness in chest–>difficulty breathing
OP poisoning irreversibly inhibits AChEsterase–>increase in ACh Tx with atropine & 2-PAM
Use of pyridostigmine
Tx of M. gravis
Use of Physostigmine
glaucoma & atropine overdose
Malathion, paration
used as insecticides parathion more toxic than malathion. Very lipid soluble & rapidly absorbed through lungs & skin
Drugs used to treat paralytic ileus
bethanechol & neostigmine
causes miosis (constriction of pupillary sphincter m)
M3
opposite of M3 in the blood vessel is
alpha 1
increases outflow of aqueous humor–>decreases IOP
M3
causes accommodation (contraction of ciliary muscle) for near vision
M3
causes mydriasis (pupillary sphincter relaxation)
alpha 1
causes urinary retention via sphincter contraction
alpha 1
opposite of M3 in the pupil is
alpha 1
reduces release of NE & consequences
alpha 2–>bradycardia, hypotension, also causes inhibition of liplysis in fat cells
results in bronchodilation
beta 2
results in bronchospasm
M3
What happens when you increase IP3 & DAG?
Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity. In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.
what’s the consequence of aldosterone secretion
aldosterone–>kidney tubules to increase sodium & water reabsorption–>increase in blood volume–>increase in BP
Opposite of M2 in the heart is
beta 1
opposite of M3 in smooth muscle is
beta 2
opposite of M3 in sphincters is
alpha 1
receptors found on blood vessels
M3 & alpha 1
receptors found in smooth muscle
M3 & beta 2
receptors found in sphincters
M3 & alpha 1
receptors found in pupils
M3 & alpha 1
receptors found in glands
M3
Receptors found in the heart
M2 & beta 1
D1 receptor 1. location 2. MOA 3. effect
- smooth muscle 2. Gs–> increase cAMP 3. relaxes renal vascular smooth muscle
Reflex response to a drop in blood pressure how can you block this response?
increase in sympathetic outflow (–>increase in HR and FOC; from beta 1) and increase renin release (from beta 1; –> increase salt and water retention) and decrease in parasympathetic you can block this with ganglion-blocking drugs i.e. hexamethonium
what happens in juxtaglomerular cells when renal blood flow decreases
- JG cells convert prorenin (found in blood) to renin and secrete it into circulation 2. renin converts angiotensinogen (secreted by liver) to angiotensin 1 3. AT1–>AT2 by ACE (found in lungs) 4. AT2–> BV constriction–>increase in BP 5. AT2 also stimulates secretion of aldosterone from the adrenal cortex 6. aldosterone–>kidney tubules to increase sodium & water reabsorption–>increase in blood volume–>increase in BP
DAG modulates
DAG modulates action of PKC
IP3 leads to
IP3–>Ca2+ release from intracellular storage–>sm contraction
from where is angiotensinogen secreted?
liver
where is ACE found
lungs
what does AT2 do?
- AT2–>BV constriction–>increase in BP 2. AT2 also stimulates secretion of aldosterone from the adrenal cortex)
from where is aldosterone secreted?
adrenal cortex (AT2 also stimulates secretion of aldosterone from the adrenal cortex)
In ANS preganglionic fibers, ACh acts through ___ receptors?
Nn
does neostigmine have nicotinic, muscarinic or both activity
both (all indirect, reversible cholinergic agonists do)
drug used to treat atropine overdose
physostigmine
D1 receptor location
smooth muscle
D2 receptor location
nerve endings
beta 2 affect on the human liver
activates glycogenolysis
bc increases pancreas insulin secretion
alpha 2 affect on fat cells
inhibition of lipolysis
alpha 1 affect on the prostate
causes contraction in ductus deferens and seminal vesicles –>ejaculation
alpha 2 affect on vascular smooth muscle in the nasal mucosa
nasal decongestion
beta 2 affect on skeleton muscle
promotes potassium uptake
also causes vasodilation of the vascular beds in skeletal muscle which –> decrease in TPR
2 ways in which adrenergic system can affect PVR
- alpha 1–>vasoconstriction–>increases TPR–> increases BP
- beta 2–>vasodilation–> decreases TPR–> decreases BP
receptors that act on fat cells and their actions
beta 3: activates lipolysis
alpha 2: inhibites lipolysis
