Lectures: ANS 5-8 Flashcards
selectivity of Alpha adrenergic R subclass
1. epinephrine
- norepinephrine
- (much less) isoproterenol
neurotransmission steps affected by adrenergic agonist drugs
Direct-acting: bind to the post-synaptic receptor
In-direct:
- induce release of NE into synapse
- limit re-uptake of NE from synapse
selectivity of beta adrenergic R subclass
1. isoproterenol
- epinephrine
- norepinephrine
(2 & 3 are almost same affinity)
effects of alpha-1 adrenergic R activity
- increase BP (vasoconstriction @ skin, renal, splanchnic, lungs)
- decrease congestion
(decrease mucus secretion in upper respiratory tract) - mydriasis (pupillary radial/dilator mm contraction)
effects of alpha-2 adrenergic R activity
decrease BP (via central sympathetic vasomotor center) --> agonists = anti-hypertensives * Also: some a2 Rs = on PRE-synaptic terminals --> inhibit NE release
effects of beta adrenergic R activity
- stimulate heart (esp. B1, –> CHF/MIs, shock, etc.)
- bronchodilate (relax lower resp. sm. muscle –> COPD/asthma)
- decrease uterine contractions (relax bladder and uterus walls)
INdirect acting adrenergic agonists
- amphetamine
- cocaine
- tyramine
(trigger AP-indep. NE release OR block reuptake)
Direct-acting adrenergic agonists (11)
- albuterol 7. phenylephrine
- clonadine 8. methoxamine
- dobutamine 9. isoproterenol
- dopamine 10. salmeterol
- Epinephrine 11. tertbutaline
- norepinephrine
catecholamines (list)
- epinephrine
- norepinephrine
- dopamine
- dobutamine
- isoproterenol
non-catecholamines (list)
- albuterol 5. methoxamine
- clonadine 6. salmeterol
- ephedrine 7. tertbutaline
- phenylephedrine 8. amphetamine*
catecholamines (characteristics)
- Duration of action: short
- CNS absorption: poor
- metabolized by COMT/MAO? Yes!
- Route of administration: Not oral
non-catecholamine adrenergic agonist (characteristics)
- Duration of action: Long
- CNS absorption: HIGH
- metabolized by COMT/MAO? not well
- Route of administration: may be oral
Beta-2 specific adrenergic agonists
Beta-1: dobutamine
Beta-2: albuterol, salmeterol, tertbutaline
- most other adrenergic agonists = mixed selectivity
alpha specific adrenergic agonists
alpha-1: methoxamine
alpha-2: clonidine
- most other adrenergic agonists = mixed selectivity
shock (Sx &Tx)
cardiovascular syndrome w/ hypotension, altered mental state, and metabolic acidosis (Sx)
Treatment: increase tissue perfusion, treat cause #1 Dopamine... 2. norepinephrine
neurotransmission steps affected by adrenergic antagonist drugs
Mostly only affects post-synaptic receptor binding
*but: Reserpine blocks uptake into vesicles
general effects of alpha-1 adrenergic antagonists
- vasodilation –> decrease BP
- smooth muscle relaxation –> relax prostrate/bladder sphincter
==> useful for:
pheochromocytoma, Reynauld’s disease, HTN, BPH
general effect of beta adrenergic antagonists
- decrease CO by block cardiac stimulation
–> for reducing heart strain after MI,
& reduce exercise-related angina - decrease BP –> for HTN, hyperthyroidism
- decrease intraocular pressure –> for glaucoma
Beta adrenergic R antagonists (list)
- acebutolol 5. nadolol
- atenolol 6. pindolol
- esmolol 7. propanolol
- metroprolol 8. timolol
* 9. labetAlol (alpha & beta)
alpha adrenergic R antagonists (list)
(all cause BIG decrease BP –> reflex increase CO)
a-1 selective: (2)
phentolamine, phenoxybenzamine (irrreversible!)
Non-selective: (3)
doxosin, prazosin, terazosin
pheochromocytoma
a tumor of the adrenal medulla which secretes NE, Epi, and/or Dopamine.
–> increases risk of heart problems (MI, arrhythmias, CHF, stroke, pulmonary edema)
Sx: HTN, severe headache, profuse sweating
Treatment: phenoxybenzamine & phentolamine, or labetalol
Reynauld’s disease
condition of reduced blood flow to hands spontaneously or after cold stimulus, causing ischemia/cyanosis/erythema.
–> risk of: finger wasting, necrosis/gangrene, ischemic ulcers
treatment:
prazosin/doxosin/terazosin, and phenoxybenzamine
(increase perfusion by BLOCK vasoconstriction)
effects of giving phentolamine BEFORE Epi/NE
for NE: blocks increase in PVR –> limits NE effect to direct heart effects only (blocks BP change and assoc. reflex changes)
for Epi: –> DEcrease dBP and CO, and aungments reflex response –> increases HR and contractility
Benign Prostatic Hypertrophy/hyperplasia (“BPH”)
enlarged prostate compresses bladder & makes difficult to urinate and empty bladder.
Sx: strong urge, frequent urination, weak passage of urine, burning on urination, distention
Treatment: doxazosin/terazosin (relax sm. muscle)
relative duration of action of beta adrenergic antagonists
minutes (shortest): esmolol (only by IV)
hours: acebutolol, metoprolol, pindolol;
propanolol, timolol, atenolol, labetalol
day (longest): nadolol
“ISA” (Intrinsic Sympathomimetic Action)
= a drug that acts as a partial agonist,
blocks the endogenous NE/Epi/Dopamine, but simultaneously (weakly) stimulates the target receptor.
ie: pindolol & acebutolol
(beta adrenergic antagonists)
beta adrenergic R antagonists w/ local anesthetic f(x)
= direct block of voltage-gated Na+ channels,
- propanolol
- pindolol
- acebutolo
- metoprolol
- labetalol
beta-1 R specific adrenergic antagonists
- especially good for treating HTN/angina in special case patients
(ie: asthma/COPD, diabetes) bc has much less effect on lungs and metabolism (B2 Rs).
1. Acebutolol
2. Atenolol
3. Esmolol
4. Metroprolol
