Sympathetic Nervous System Pharmacology Flashcards
CPCRs
activate second messengers and exnymes within the cell
catecholamines
dopamine
NE
Epi
(all derived from tyrosine)
NE
release from sympathetic neurons
NE and Epi
relatively equivalent, except NE has low potency for B2 rec
sympathomimetic
enhance signalling
sympatholytic
decrease signaling
adrenergic receptors in the brain
central noradrenergic system that originate in the brain stem and release NE to activate adrenergic receptors thorughout brain
effects of adrenergic receptors in brain
attention, arousal, wakefulness, anxiety, memory formation
can peripheral NE and EPi cross BBB?
no
but many adrenergic drugs do. therefore, can regulate brain adrenergic receptors to produce therapeutic and unwanted side effects
reflex bradycardia
low HR is compensation, reflex response to drug administered (response to vasoconstriction)
reflex tachycardia
histamine –> decrease BP –> increase HR for compensation (response to dilation)
alpha 1 receptors
-cause Ca2+ release
-stimulate smooth muscle contraction
-vasoconstriction
-mydriasis
Alpha 2 receptors
-presynaptic
-inhibits Nt release
-reduce BP
-decrease in sympathetic outflow
beta 1 receptors
increase HR and contractibility
beta 2 receptors
-dilate / relax smooth muscle along respiratory tract and BV (bronchodilation)
-vasodilation in skeletal msucles
beta 3 receptors
-lipolysis in adipocytes (release energy reserves)
4 alpha adrenergic agonists
epinephrine
phenylephrine
oxymetazoline
clonidine
epinephrine
-vasoconstrictor with local anesthetic
phenlyephrine
-a1 selective
-decongestant
oxymetazoline
-a1 selective
-decongestant
overuse of oxymetazoline in short term
rhinitis medicamentosa
rebound congestion (more congestion than before)
overuse of oxymetazoline in long term
turbinate hypertrophy
enlargement of bone and tissue in airway
clonidine
a2 selective
-decrease sympathetic outflow, reduce BP
-decrease NE release because autoreceptor on presynaptic terminal