SNS drugs Flashcards
where are andrenergic receptors found
- CNS and SNS
2. presynaptically on neuron or post-synaptically on effector organ
where do catecholamines come from
synthesized from tyrosine in sympathetic nerve endings
what are drugs that turn on SNS
- sympathicomimetics
2. a or B angonists
what are drugs that turn off SNS
- sympatholytics
2. a or B blockers
what are receptor types for each SNSr
a1 - Gq and i/o
a2 - Gi/o
B - Gs
tissues for a1
- vascular smooth muscle
- GU and GI smooth muscle
- heart
- liver
tissues for a2
- pancreatic B cells
- platelets
- nerve
- vascular smooth muscles
actions of a1 agonists
- vasoconstriction
- increased vascular resistance
- enlarged pupils
- sphincter closure
actions of a2 agonists
inhibit cAMP
- inhibits Ca channels , NE release, Ach release, insulin release
tissues for B1
- heart
2. juxtaglomerular cells
tissues for B2
- bronchi
- skeletal muscle
- liver
tissues for B3
- adipose
actions of B1 agonists
Gs > cAMP> opening of Ca channel - contractions
- tachycardia
- myocardial contraction
- lipolysis
- renin release
actions of B2 agonists
Gs > cAMP > PKA phosphoylate MLCK > inactive > relax
- vasodilation
- decrease peripheral resistance
- bronchodilation
- glycogenolysis
- release of glucagon
3 potential actions of sympathomimetics
- direct action - stim G receptor
- indirect - affect synthesis, storage, release of actitivy
- mixed
what are direct acting sympathomimetics (2)
catechoamines 1. rapid onset 2. breif action 3. paraenterally non - catecholamines
5 important catecholamines
- NE
- E
- dopa
- isoproterenol
- dobutamine
where does NE act and what does it do (2)
- a>B1»B2,3
- increase MAP and PVR
- increase HR but reflex bradycardia
where does E act and what does it do (2)
- low dose mostly B and high dose mostly a
2. increase inotropy and chronotropy (B1), bronchodilates (B2), hyperglycemia, drops peripheral resistance (B2)
what does dopamine do
- vasodilates peripheral renal, mesenteric, coronary vascular beds via D1
- inhibs NE release
- at high does B1 effects the biggest
- at higher dose a1 is most - good for treatment of shock
what are a1 agonists (phenyephrine) used for
treatment of shock, nasal decongestants
what are a2 agonists (clonadine) used for
hypertension by acting on CNS to inhibit sympathetic output
- CNS - inhibits excitatory outflow
- peripheral - inhibits release of catecholamines
what are B1 agonists (dobutamine) used for
increase cardiac output - ionotropic effects more significant
what are B2 agonists (salbutamol) used for
aerosols for bronchodilation
what is a non-seletive B agonist
isoproterenol
- most prominent effects are B, but rarely used because of lack of selectivity
what does and indirect andrenergic agonist (amphetamine) do
reverses the vesicular monoamine transporter > more NE and dopa
- vasoconstriction, MAP, ionotropy
- wakefulness, euphoria, anxiety, hypertension
what are mixed sympathomimetics
ephedrine and pseudoephedrine
- increase release of NE and stim a1, B1, B2
2 classes of sympatholytics and examples
- direct - a and B blockers
2. indirect - decrease release, change storage, decrease synthesis
2 types of a blockers
- reversible - can be displaced by agonists - phenotolamine, prazolin
- irreversible - covalent bond - phenoxybenzamine
what do non-selective a blockers do
- both a1 and a2
- lower PVR and reflex tachycardia
- more profound effects when standing
- more NE released because of a2 blockade
what do a1 selective blockers do
- good for hypertension
- lower PVR
- fewer adverse effects
- lower lipid levels
- ___-zosins
what do a1A selective blockers do
- tamulosin
- treatment of BPH by causing vasodilation of the prostate vascular smooth muscle
what are effects of non-selective B-blockers (propranolol)
- lower ionotropy, chronotropy, CO, SA and AV activity
- brochoconstrict problematically
what are B1 blockers good for
avoid bronchoconstriction
- metoprolol, atenolol, bisprolol
