Exam 2: Bosco Lectures: Autonomic Drugs Flashcards
Lecture 14 and 15
Name some adrenergic agonists: alpha and beta 1 and 2
α1 = EPI, NE, phenylephrine
α2 = Medetomidine
β1 = EPI, NE, dopamine, dobutamine
β2 = bronchodilation EPI, albuterol, clenbuterol
Lecture 12
What are the four ways that NT can be metabolized and which NT is dominant in the PNS and its main form of metabolism?
reuptake, uptake, degradation, diffusion.
Acetylcholine dominates the parasympathetic division and is metabolized via degradation.
Lecture 12
What is NANC transmission?
Smooth muscles innervated by ANS
some ANS effects in the presence of adrenergic and cholinergic blockade.
Non-adrenergic, non-cholinergic transmission
primarily inhibitory effects
Purinergic neurotransmission
adenosine receptors (P1)
ATP receptors (P2X and P2Y)
ATP often released as a co-transmitter with ACh or NE
Nitric oxide
AKA endothelium-derived relaxation factor
nitrergic nerves
talk about this more later
Lecture 12: ANS target organ effects
How does sympathetic and parasympathetic affect the heart, blood vessels, lungs, GI, urinary bladder, eye, salivary glands and autonomic nerve endings?
- Heart
sympathetic (B1): increase cardiac output
parasympathetic (M2): decrease cardiac output - Blood vessels
sympathetic (a1 constriction, B2 dilation): directs blood flow to skeletal muscles
parasympathetic (M3): no/little innervation - Lungs
sympathetic (B2): increase ventilation
parasympathetic (M3,M2): decrease ventilation - Gastrointestinal system
sympathetic: decrease activity
parasympathetic (M3, M2): increase activity - Urinary bladder
sympathetic: inhibit voiding
parasympathetic (M3): promote voiding - Eye
sympathetic (midriasis a1, aqueous humor B2): enhance vision
parasympathetic (M3,M2): limit vision - Salivary glands
sympathetic: small increase in viscous secretions (minimal)
parasympathetic (M3,M2): increase watery secretions - Autonomic nerve endings
sympathetic (a2) and parasympathetic: limit NT release (autoreceptors and heteroreceptors)
Lecture 12: Direct acting (and endogenous) cholinergic agonists
Acetylcholine
Rarely used clinically (ophthalmic)
muscarinic and nicotinic stimulation
rapid degradation by AChE and plasma butyrylcholinesterase
Lecture 12: Direct acting cholinergic agonists
Muscarine
Muscarine (an alkaloid)
stimulates muscarinic receptors
not used clinically
found in certain mushrooms (contributes to some cases of mushroom poisoning)
Lecture 12: Direct acting cholinergic agonists
Pilocarpine
Pilocarpine (an alkaloid)
muscarinic stimulation
topical ophthalmic used to induce pupil constriction and decrease intraocular pressure during glaucoma
rarely used systemically to promote salivation (sialogogue)
Lecture 12: Direct acting cholinergic agonists
Bethanechol
Bethanechol (synthetic choline ester)
muscarinic stimulation, some GI / urinary bladder selectivity (some M3 selectivity)
promotes voiding by contraction of the detrusor and relaxation of the trigone and sphincter
used to treat urinary retention when obstruction is absent.
Lecture 12: Indirect acting cholinergic agonists
Physostigmine and Neostigmine
- stimulate visceral smooth muscle (neostigmine)
- counter anticholinergic toxicity (physostigmine)
**Acetylcholinesterase (AChE) inhibitors
**
prevent hydrolysis of acetylcholine to choline and acetate, the primary mechanism terminating ACh signaling
**accumulation of ACh at sites of release: **
autonomic effector organs and ganglia, skeletal muscle, cholinergic synapses in the CNS
“reversible” covalent inhibitors: physostigmine (a quaternary compound that can cross the blood-brain barrier), neostigmine, and pyridostigmine
Clinical uses of “reversible” covalent inhibitors:
* smooth muscle atony (GI tract and urinary bladder)
* glaucoma (topical)
* reversal of competitive non-depolarizing neuromuscular blocking agents (more later)
* myasthenia gravis (ACh receptor deficiency)
* counter CNS symptoms of anticholinergic intoxication (physostigmine)
“Irreversible” covalent inhibitors:
* organophosphate compounds
* insecticides (e.g. malathion)
* “nerve gases” (e.g. sarin)
What is the general synaptic organization, major receptors and neurotransmitters of the autonomic nervous system?
parasympathetic, sympathetic, and somatic
The symapthetic nervous system: CNS releases ACh to nicotinic cholinergic receptors that release NE to alpha and beta receptors and a nictotine receptor in the adrenal medulla that release E to the blood to reach alpaha and beta receptors.
The CNS of the parasympathetic nervous system releases Ach to nicotinic receptors that release Ah to Muscarinic receptors.
The somtatic system, the CNS releases Ach to Nitcotinic recptors and it ends there.
How is acetylcholine and norepinephrine/epinephrine metabolized?
ACh mainly degredation by AChE
Catecholamines are metabolized from tyrosine to dopa to dopamine to NE to E. They are not degraded but can undergo uptake, reuptake and diffusion. NET reuptakes NE
What are the general receptor signal transduction mechanisms of nicotinic, muscarinic, cholinergic, and adrenergic receptors?
Nicotinic cholinergic receptors
are a ionotropic ligand-gated cation channel. ACh binding opens the channel pore to cause a sodium influx which leads to depolarization. Nicotinic receptors excite post-synaptic neurons
Muscarinic cholinergic receptors M1 – M5 Inhibit or excite postsynaptic neurons. Adrenergic alpha receptors have α1 and α2 and Adrenergic beta receptors have β1 and β2 (and β3). All of these are G protein coupled receptors. Alpha receptors are mostly involved in the stimulation of effector cells and constriction of blood vessels. On the other hand, beta receptors are mostly involved in the relaxation of effector cells and dilatation of blood vessels
depolarize = more positive
acetylcholine (direct; endogenous)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Acetylcholine
Rarely used clinically (ophthalmic)
muscarinic and nicotinic stimulation
rapid degradation by AChE and plasma butyrylcholinesterase
*reverse NMJ blockade (AChE inhibitors)
bethanechol (direct; some M3 selectivity)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Bethanechol (synthetic choline ester)
muscarinic stimulation, some GI / urinary bladder selectivity (some M3 selectivity)
promotes voiding by contraction of the detrusor and relaxation of the trigone and sphincter
used to treat urinary retention when obstruction is absent.
*empty urinary bladder
Muscarine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Muscarine (an alkaloid)
stimulates muscarinic receptors
not used clinically
found in certain mushrooms (contributes to some cases of mushroom poisoning)
Pilocarpine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Pilocarpine (an alkaloid)
muscarinic stimulation
topical ophthalmic used to induce pupil constriction and decrease intraocular pressure during glaucoma
rarely used systemically to promote salivation (sialogogue)
*induce miosis in the eye
physostigmine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Clinical uses of “reversible” covalent inhibitors:
smooth muscle atony (GI tract and urinary bladder)
glaucoma (topical)
reversal of competitive non-depolarizing neuromuscular blocking agents (more later)
crosses the blood-brain barrier
*counter anticholinergic toxicity
neostigmine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Clinical uses of “reversible” covalent inhibitors:
smooth muscle atony (GI tract and urinary bladder)
glaucoma (topical)
reversal of competitive non-depolarizing neuromuscular blocking agents (more later)
*stimulate visceral smooth muscle
glycopyrrolate
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Glycopyrrolate (synthetic)
Similar to atropine but quaternary so Does not cross BBB: little CNS effects
Used as adjunct to general anesthesia
decrease salivary and airway secretions
prevent vagally-mediated bradycardia
*decrease secretions, prevent bradycardia
quaternary: to big to cross BBB
ipratropium
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Ipratropium
↓ bronchoconstriction and airway secretions
Quaternary: restricted distribution, administer via inhalation, limit systemic effects
Uses for asthma (cats) and chronic bronchitis (dogs) and horses with recurrent airway inflammation
*promote bronchodilation
scopolamine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
atropine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Atropine (natural alkaloid)
Competitively inhibits the binding and stimulation of muscarinic receptors by ACh and other muscarinic agonists
Prototypical anticholinergic isolated from Atropa belladonna (deadly nightshade)
Used as adjunct during general anesthesia to decrease salivary and airway secretions
*decrease secretions
propantheline
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Propantheline
**↓ detrusor contraction
↑ trigone and sphincter contraction **
promotes urine retention
Uses:
treat incontinence due to detrusor instability
*promote urine retention
tropicamide
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Tropicamide (synthetic)
Used topically in the eye to produce mydriasis and cycloplegia (loss of ability to maintain focus on an object as it draws near the eye) in an ophthalmic examination and has a shorter duration of action than atropine
*induce mydriasis & cycloplegia
epinephrine (α1, β1, β2; endogenous)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Epinephrine (AKA adrenaline)
potent α and β agonist
released by adrenal chromaffin cells
complex action: summation of α and β agonist activity
cardiovascular effects (very important)
Cardiac effects (β1)
↑ contractility (positive inotrope)
↑ heart rate (positive chronotrope)
↑ O2 consumption
general result: ↑ cardiac output (CO)
Vascular effects
↓ **cutaneous, visceral, renal blood flow via vasoconstriction **(α1)
↑ skeletal muscle blood flow via dilation (β2)
Vascular effects are dose dependent
Can be given IV, IM or subcutaneously (not orally active)
Respiratory effects (important):
powerful bronchodilator (β2)
especially if bronchioles pre-constricted
e.g. anaphylaxis or asthma
small decrease in bronchial secretions
Rapid relief of hypersensitivity reactions (e.g. anaphylaxis and asthma) cardiovascular support (e.g. BP) and bronchodilation.
Restoring cardiac rhythm during cardiac arrest or an atrioventricular (AV) node block
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
norepinephrine (α1, β1; endogenous)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Major NT released by post-ganglionic sympathetic nerves
AKA noradrenaline
Differs from epinephrine by lacking a single methyl group
NE is a direct α and β receptor agonist (as with EPI)
NE and EPI have different potencies on α and β receptors
* β1: EPI ≈ NE
* β2: EPI»_space;»> NE
* α1: EPI > NE
NE effects and toxicity similar to EPI in most respects:
differences result from lack of β2 stimulation
intense vasoconstriction and increase in blood pressure,
initiates baroreceptor reflex (negative feedback mechanism) which slows heart rate
Limited use
cardiovascular support (maintain BP) during shock via α1 (vasculature) and β1 (heart) effects
Sometimes used during cardiac resuscitation
Minimal β2 effect = no bronchodilation
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
dopamine (D1, β1, (α1); endogenous)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Endogenous catecholamine
Precursor to NE and EPI
Given IV (infusion), short half-life
DOSE DEPENDENT EFFECTS:
low dose (1-10 µg/kg)
stimulates vascular** D1 dopamine receptors**
coupled to Gαs = ↑ cAMP = vasodilation
** increased renal blood flow and sodium excretion**
stimulates cardiac β1 receptors
**positive inotropic effect **
Higher dose (>10 µg/kg): stimulate vascular α1 receptors, vasoconstriction, ↓ renal blood flow, etc.
Use low dose IV infusion for congestive heart failure with compromised renal function - short term only
Often used to treat hypotension during anesthesia
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
dobutamine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Dobutamine
structurally related to dopamine
available as a racemic mixture of optical isomers with different properties
complex agonist activity on β1, β2 and α1 receptors (β1 > β2 and α1)
(but not D1 receptors as with dopamine)
Dobutamine cardiovascular effects:
increased cardiac contractility (β1 agonist) with minimal changes in heart rate
minimal change in BP as α1 and β2 agonist activities are weaker and counterbalance
use as positive inotrope during heart failure (IV only, short term)
General adverse effects/toxicity of non-selective β agonists: unwanted and/or excess β stimulation, e.g. ↑ HR (β1) when used as bronchodilator (β2)
nonselective but acts selective
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
albuterol
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Albuterol (AKA salbutamol)
for bronchospasm in dogs, cats, horses
selective B2 adrenergic agonists
β2 agonist = bronchodilator
Gαs = ↑ cAMP = relax bronchial smooth muscle
Cardiovascular effects (i.e. stimulation) less evident than with the non-selective β agonist isoproterenol
minimize further with aerosol administration
General adverse effects/toxicity of selective β2 agonists
unwanted and/or excess β stimulation
tremor, restlessness, cardiac excitation (β1)
minimize with inhalation
β receptor down-regulation
following chronic, long-term administration of β agonists (especially with over-usage)
leads to loss of pharmacological efficacy
minimize with proper dose, dosing schedule
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
clenbuterol
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Clenbuterol
used for allergic bronchitis, recurrent airway obstruction (“heaves”), and broncho-constriction in horses
selective B2 adrenergic agonists
β2 agonist = bronchodilator
Gαs = ↑ cAMP = relax bronchial smooth muscle
Cardiovascular effects (i.e. stimulation) less evident than with the non-selective β agonist isoproterenol
minimize further with aerosol administration
General adverse effects/toxicity of selective β2 agonists
unwanted and/or excess β stimulation
tremor, restlessness, cardiac excitation (β1)
minimize with inhalation
β receptor down-regulation
following chronic, long-term administration of β agonists (especially with over-usage)
leads to loss of pharmacological efficacy
minimize with proper dose, dosing schedule
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
phenylephrine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Primary effect of α1 stimulation is constriction of vascular smooth muscle
increased total peripheral resistance
increased blood pressure (pressor agents)
limited use in hypotension and shock
nasal decongestant (systemic & topical)
Phenylephrine
prototypical α1 agonist
topical, oral, parenteral
**decongestant, vasopressor **
Methoxamine, metaraminol, mephentermine, midodrine
Toxicity = excess α1 activity (hypertension)
*α1 = vasoconstrictor
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
medetomidine
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
selective a2 adrenergic receptors
Effect primarily central (CNS) and pre-synaptic inhibition of sympathetic neurons
sedation, analgesia
decreased sympathetic outflow from brain
decreased NE release
↓ sympathetic activity
(CNS inhibition)
(Dex)medetomidine & xylazine
α2 agonists = CNS depression
widely used as adjunct for sedation, anesthesia, and analgesia in veterinary medicine
pre-anesthetic, light anesthesia by itself
relatively high safety profile (i.e. therapeutic index)
allows for a lower dose of other anesthetic/analgesic agents with lower safety profiles
Overall effect is a decrease in blood pressure (and sedation/analgesia)
stimulation of pre-synaptic α2 receptors
Transient increase in blood pressure
stimulation of post-synaptic α2 receptors on arterial smooth muscle cells
*α2 = sedative, also decreases sympathetic outflow
(also xylazine)
α1 = vasoconstriction (EPI, NE, phenylephrine)
α2 = presynaptic inhibition (medetomidine)
β1 = ↑ HR and contractile force (EPI, NE, dopamine, dobutamine)
β2 = bronchodilation (EPI, albuterol, clenbuterol)
phenoxybenzamine (α1, α2; non-competitive)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Non-selective α antagonists
irreversibly blocks α1 and α2 receptors
Phenoxybenzamine, phentolamine
non-selective α antagonists
reduces urethral sphincter tone
manage urethral blockage
α1 antagonist = vasodilation (prazosin)
α2 antagonist = reverse α2 agonists
atipamezole reversal of medetomidine
non-selective α antagonists
phenoxybenzamine (non-comp, irreversible)
phentolamine (competitive, reversible)
phentolamine (α1, α2; competitive)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Direct acting competitive antagonists
reversibly block the stimulation of α and β receptors by endogenous NTs
varying degree of selectivity at different receptors
most adrenergic antagonists
Non-selective α antagonists
reversibly blocks α1 and α2 receptors
Phenoxybenzamine, phentolamine
non-selective α antagonists
reduces urethral sphincter tone
manage urethral blockage
α1 antagonist = vasodilation (prazosin)
α2 antagonist = reverse α2 agonists
atipamezole reversal of medetomidine
non-selective α antagonists
phenoxybenzamine (non-comp, irreversible)
phentolamine (competitive, reversible)
prazosin (α1)
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Prazosin, terazosin, doxazosin
major effect is to relax arterial and venous smooth muscle = vasodilation
decrease in total peripheral resistance (after-load)
decrease in venous return (pre-load)
used as antihypertensive and in congestive heart failure (reduced pre-and after-load)
produce less reflex tachycardia than other vasodilation agents
prominent postural (orthostatic) hypotension in humans at start of therapy (1st dose-effect)
In vet med, most commonly used to treat urethral spasm in cats and dogs
α1 antagonist = vasodilation (prazosin)
α2 antagonist = reverse α2 agonists
atipamezole reversal of medetomidine
non-selective α antagonists
phenoxybenzamine (non-comp, irreversible)
phentolamine (competitive, reversible)
Atipamezole
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
sleective a2 adrenergic antagonists:
Antagonist effect primarily relieving central (CNS) and pre-synaptic inhibition
less sedation, analgesia
increased sympathetic outflow from brain
increased NE release
↑ sympathetic activity
↓ CNS inhibition
Atipamezole, yohimbine
selective α2 antagonists (competitive)
used to reverse sedative and analgesic effects of medetomidine (α2 agonist)
clinical reversal (i.e. planned)
toxicological reversal (i.e. not planned)
Rapid reversal of sedation (minutes) with minimal risk for relapse into sedation
Consider half-life of each.
atipamezole ≈ 2X that of medetomidine
timing, species differences
do not want re-sedation
**also increases sympathetic activity
**
do not use in patients with cardiac and respiratory disease or other conditions where excessive sympathetic stimulation is contraindicated
α1 antagonist = vasodilation (prazosin)
α2 antagonist = reverse α2 agonists
atipamezole reversal of medetomidine
non-selective α antagonists
phenoxybenzamine (non-comp, irreversible)
phentolamine (competitive, reversible)
Propranolol
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
nonselective B adrenergic antagonists:
Propranolol
prototypical β antagonist with equal affinity for β1 and β2 receptors
decreases cardiac output (β1 blockade)
more pronounced during exercise (increased sympathetic tone)
antiarrhythmic action from decreased sympathetic stimulation and non-adrenergic effects (e.g. “membrane stabilization”)
limited use because of β2 blockade and availability relatively selective β1 inhibitors
β1 antagonists: decrease heart rate
propranolol (non-selective), atenolol (selective)
decrease heart rate, reduce cardiac oxygen demand, decrease blood pressure
β2 antagonists: bronchoconstriction
propranolol (non-selective)
not helpful, limitation of non-selective agents
timolol
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
Timolol: ocular use to decrease aqueous humor production during glaucoma
nadolol, penbutolol, pindolol, etc. etc.
carvedilol, labetalol, bucindolol: also block α1 receptors (plus multiple other effects).
atenolol
- generic name and drug class (i.e. what receptors they influence)
- target organ effects (desired and undesired)
- general clinical considerations (emphasize critical care)
selective B1 adrenergic antagonists:
Selectivity is relative, block β2 receptors at higher doses.
Advantage: safer to use in patients with bronchospastic disease.
Atenolol, metoprolol, acebutolol, esmolol, etc., etc.
Decreased heart rate and cardiac contractility.
↓ cardiac output, ↓ cardiac oxygen demand
BP = CO x PR, ↓ blood pressure
excessive sympathetic stimulation is pro-arrythmogenic, ↓ cardiac arrhythmias
potentially useful in feline hypertrophic cardiomyopathy (↓ HR, oxygen demand, etc.)
newer concept
beta blockers used to be contraindicated in heart failure
decreased heart rate
counteract anticholinergic tachycardia
anticholinergic toxicity (e.g. atropine)
e.g. during pancuronium NMJ block
β1 antagonists: decrease heart rate
propranolol (non-selective), atenolol (selective)
decrease heart rate, reduce cardiac oxygen demand, decrease blood pressure
β2 antagonists: bronchoconstriction
propranolol (non-selective)
not helpful, limitation of non-selective agents
