Adrenergic lecture Flashcards
SNS
Organ systems, blood pressure
Hormone vs. neurotransmitter
Adrenal medulla
NT Termination
Acetylcholine
(2)
ACh-esterase
150ms
NT Termination
Norepinephrine
(3)
Reuptake
Monoamine oxidase
Catechol-O-
Methyltransferase
sympathetic agonists
Direct
(3)
Route
Affinity
Expression of receptor subtypes
sympathetic agonists
Indirect
(2)
Catecholamine displacement
Amphetamines
Decreased NE clearance
Reuptake inhibition
adrenergic receptors
(4)
α1 α2
β1 β2
Dopamine
Sympathomimetic vs sympatholytic
adrenergic receptors
Can be downregulated / desensitized
(3)
Congestive Heart Failure (CHF)
Acidosis
Hypoxia
α1
(6)
Peripheral vascular beds
Excitatory
Vasoconstriction
Blood pressure increased
Mydriasis
Urinary sphincter constriction
α2
(6)
Inhibitory
In the vasculature
Inhibition of NE and ACh
Decreased sympathetic tone
Decreased BP
Sedation
β1
(3)
Excitatory
Cardiac excitation
Increased rate, contractility,
conduction
β2
(5)
Inhibitory
Bronchodilation
Smooth muscle relaxation
Skeletal muscle vasodilation
Decreased vascular resistance
DA
Resistance vessel vasodilation
(4)
Renal
Splanchnic
Coronary
Cerebral
Primary catecholamines
Dopamine (DA) and
norepinephrine (NE)
DA –
NE –
Epinephrine –
Brain and kidney
Sympathetic nerve endings
Adrenal medulla
norepinephrine
a1, b1, b2
Endogenous
Primary neurotransmitter at sympathetic nerve endings
Maintenance of sympathetic tone
BP
No cardiac output changes
Minimal chronotropic changes
Increased coronary blood flow
Caution with prolonged infusions
epi
@ higher doses
@ lower doses
@ lower doses
α1
β1
β2
epi
Endogenous
Only released by adrenal medulla
Stress preparation
coronary blood flow
Caution prolonged infusions
DA
α1
β1
β2
Endogenous
NE precursor
Dose-specific effects
Low dose (0.5 – 3 mcg/kg/min)
Intermediate (3 – 10 mcg/kg/min)
High (10 – 20 mcg/kg/min)
dobutamine
β1
β2
α1
Synthetic
Augments myocardial contractility
Dose-dependent increase in stroke volume (SV) and cardiac output (CO)
Alpha agonist AND antagonist
Beta-mediated vasodilation (low dose)
High dose increases myocardial O2 consumption
phenylephrine
α1
Synthetic
All alpha, no beta
Not a catechol derivative, not
metabolized by COMT
Can lead to baroreceptor-mediated
decrease in HR
Push dose pressor