Adrenergic Pharm Flashcards
Where do adrenergic drugs take effect?
SNS
- a and B receptors (NE) - cardiac muscle, smooth muscle, glands, nerve terminals
- D1 receptors (dopamine) - renal vascular smooth muscle
Where do cholenergic drugs take effect?
PNS
*MAChR (ACh) - cardiac muscle, smooth muscle, glands, nerve terminals, sweat glands
Are sweat glands under sympathetic or parasympathetic control?
Sympathetic
- but controlled by MAChR/ACh, and therefore affected by cholenergic drugs
- cholinomimetics and AChE inhibitors can induce sweating, anticholinergics can inhibit sweating
G protein and effects of
a1 receptors
Gq, increased IP3, DAG
*increased Ca actvates PKC
G protein and effects of
a2 receptors
Gi, decreased cAMP
*decreased PKA activity
G protein and effects of
B receptors
Gs, increase cAMP
*increased PKA activity
G protein and effects of
D1 receptors
Gs, increase cAMP
*increased PKA activity
G protein and effects of
D2 receptors
Gi, decrease cAMP
*decreased PKA activity
Phenylephrine MOA
a1 agonist
Clonidine MOA
a2 agonist
Dobutamine MOA
B1 > B2 agonist
Isoprotenol MOA
B1 = B2 agonist
Albuterol MOA
B2 > B1 agonist
Effects of a1 activation
*Phenylephrine, Norepinephrine
Vasoconstriction
*agonists can cause reflex bradycardia (phenylephrine, norepinephrine)
Effects of a2 activation
*Clonidine
Sympatholytic, decreased BP and HR
*also cause platelet aggregation
Effects of B1 activation
Increased HR and contractility, increased renin release
Effects of B2 activation
Respiratory, uterine and vascular smooth muscle relaxation
- K+ uptake in skeletal muscle
- Gluconeogenesis and glycogenolysis in liver
Effects of B3 activation
Relaxation of detrusor muscle
Effects of D1 activation
Dilates renal vasculature
Effects of D2 activation
modulates neurotransmitter release in brain
Effects of epinephrine
- Increased HR and contractility (B1)
- Increases SBP, decreases bronchial secretions (a1)
- Decreases DBP, relaxes bronchial SM, muscle tremor due to K+ uptake, liver glycogenolysis and gluconeogenesis (B2)
Adrenergic receptors found in the skin and mucous membranes
mostly a1
Adrenergic receptors found in the skeletal muscle
a1 and B2
Adrenergic receptors found in the kidneys and brain
D1 and a1
Effects of norepinephrine
- Potent vasoconstriction, increased BP (a1)
- Decreased HR (reflex bradycardia)
- Increased contractility (B1)
*no B2 effects
Effects of nonselective B agonists (B1=B2)
*Isoproterenol
- Increased HR and contractility (B1)
- Vasodilation, decreased BP (B2)
- Bronchodilation (B2)
In a patient in hypotensive emergency, what can be used to increase blood pressure?
a1 agonist effects: Norepinephrine, phenylephrine
In a patient with chronic hypotension, what can be used to increase blood pressure?
Ephedrine
*indirect adrenomimetic, increases NE and dopamine release and is direct receptor agonist
What can be given to a patient in cardiogenic shock?
Dobutamine
- B1 agonist
- can also be used short term in acute HF
What adrenomimetic can be given to treat HTN?
Clonidine
Emergency therapy for complete AV block and cardiac arrest
Epi, isoproterenol
Adrenomimetics used to help treat depression
Phenelzine, Selegiline
*MAO inhibitors
Adrenomimetics used for narcolepsy (sudden sleep attacks)
Amphetamines, methylphenidate
*Methylphenidate also used for ADHD
Adrenomimetics used for appetite suppression in obesity
Ephedrine, amphetamines
Adrenomimetic used to treat asthma
Albuterol
Adrenomimetic used to treat nasal decongestion
Phenylephrine, ephedrine
Treatment for anaphylaxis
Epi
Cocaine MOA
NE and DA reuptake inhibitor
Amphetamines, methylphenidate, tyramine MOA
Increased NE and DA release, inhibited reuptake
Ephedrine MOA
Increased NE and DA release, and direct receptor agonist
Metyrosine MOA
indirect acting adrenergic antagonist
*inhibits tyrosine hydroxylase
Guanethidine MOA
indirect acting adrenergic antagonist
*depletes and prevents storageof NE
Phentolamine, Phenoxybenzamine MOA and difference
Non-selective a1/a2 receptor antagonists
- Phentolamine non-covalent bonding and therefore shorter acting (reversible)
- Phenoxybenzamine covalent bonding and therefore longer acting (irreversible)
- treatment for catecholamine excess in pheochromocytoma
- phentolamine can also be injected into the penis to treat ED
- osin drugs MOA
* Prazosin, Tamulosin, Doxazosin
Selective a1 receptor inhibitors
Alpha antagonists used for essential HTN treatment
Prazosin, Doxazosin
*non-selective alpha blockers are NOT used for HTN (phentolamine, etc.)
Alpha antagonist used for chronic urinary obstruction in BPH
Tamulosin
*greater selectivity for a1a receptors (vs a1b), which contributes most to prostate smooth muscle contraction
Labetalol, Carvedilol MOA
Mixed B and a1 antagonists
Propanolol, Pindolol, Nadolol MOA
Non-selective B1 and B2 antagonists
Acebutolol, Betaxolol, Atenolol, Metropolol MOA
Selective B1 antagonists
B blockers that are pure antagonists
- Atenolol
- Nadolol
- Propanolol
*highest risk of bradycardia
B blockers that are partial agonists
- Acebutolol
- Labetalol
- Pindolol
*lower risk of bradycardia
B blockers that are inverse agonists
- Betaxolol
- Metropolol
*lower risk of bradycardia
B blockers used in heart failure
Metoprolol, Carvedilol
Beta blocker used in glaucoma
Betaxolol
B blocker used in hyperthyroidism
Propanolol