Flashcards in pharmacology: adrenergic drugs Deck (48):
where are alpha 1 receptors? effects?
1. radial muscle eye (contraction = mydriasis without cyclopegia@)
2. arterioles (contraction = increased TPR = increased diastolic pressure = increased afterload)
3. veins (contraction = increased venous return = increased preload = increased systolic BP)
4. bladder trigone and sphincter and prostatic urethra (contraction = urinary retention)
5. male sex organs (vas deferens = ejaculation)
6. liver (increased glycogenolysis)
7. kidney (decreased renin release - safety valve - don't want too much increase in BP)
where are alpha 2 receptors? effects?
1. prejunctional nerve terminals (decreased transmitter release and NE synthesis
2. platelets (aggregation)
3. pancrease (decrease insulin secretion)
what type of receptor is alpha 1?
Gq = increased calcium
what type of receptor is alpha 2?
Gi couples = decreased cAMP
where are B1 receptors? effects?
1. heart: oppose muscarinic 2
SA node - (increased HR (positive chronotropy))
AV node (increased conduction velocity (positive dromotrophy))
atrial and ventricular muscle (increase force of contraction (positive inotropy), conduction velocity, CO and oxygen consumption)
his-purkinje (increase automaticity and conduction velocity
2. kidney: increase renin release (complementary effect with rest of Beta 1)
what type of receptor is beta 1?
Gs coupled: increase cAMP
what type of receptor is beta 2?
Gs coupled = increased cAMP
MOSTLY NOT INNERVATED - NE CAN'T REACH!! EPI!!!!!!!
where are beta 2 receptors? effects?
1. blood vessels (all) - (vasodilation = decreased TPR = decreased diastolic pressure = decreased afterload)
2. uterus (relaxation - prevent premature labor)
3. bronchioles (dilation - relaxation)
4. skeletal muscle (increased glycogenolysis - contractility (tremor))
5. liver (increased glycogenolysis, gluconeogenesis, lipolysis)
6. pancrease (increase insulin secretion - in order to allow glucose uptake)
which receptors are most sensitive?
beta receptors! when drugs have both effects, beta responses are dominant at low doses!! alpha at higher doses
where are D1 receptors located? effects?
renal, mesenteric, coronary vasculature (vasodilation - in kidney increased RBF, increased GR, increased Na+ secretion)
fenoldopam - mechanism and clinical
D1 agonist - used for severe hypertension (causes vasodilation)
what type of receptor is D1?
Gs coupled - increased adenylyl cyclase = increased cAMP
how is potential reflex bradycardia blocked with alpha 1 agonists?
what is the direct acting alpha 1 agonist? clinical use?
phenylephrine - nasal decongestant and ophthalmologic use (mydriasis without cycloplegia)
phenylephrine effect on blood pressure
increase mean blood pressure via vasoconstriction of both arterioles and veins - no change in pulse pressure
what are the alpha 2 agonists? clinical use?
clonidine and methyldopa - mild to moderate hypertension (decrease sympathetic outflow)
what are the beta agonists? clinical use?
isoproterenol (B1=B2) - bronchospasm, heart block, bradyarrhythmias
dobutamine (B1>B2) - CHF (increased CO)
isoproterenol side effects
flushing, angina, arrhythmias
beta 1 agonist effects
increased HR, increased SV, increased CO, increased pulse pressure (d/t increase in contractility)
beta 2 agonist effects
decreased TPR, decreased BP
what are the selective beta 2 agonists? clinical uses?
salmeterol (prophylaxis asthma), albuterol (asthma), terbutaline (premature labor)
NE effect on BP
can NEVER lower BP because it has NO B2 activity
low dose epinephrine effects
B1: increased HR, increased SV, increased CO, increased PP
B2: decreased TPR and decreased BP
medium dose epinephrine effects
B1: increased HR, increased SV, increased CO, increased PP
B2: decreased TYPR, decreased BP
A1 effects!!!: increased TPR, increased BP (antagonism causes no change in BP)
high dose epinephrine effects
similar to NE = A1 predominance (increased TPR and increased BP)
how to distinguish between epinephrine and NE
CANNOT distinguish based on cardiovascular - bronchioles dilated with epi
what are the beta 2 specific effects
smooth muscle relaxation; bronchioles, uterus, blood vessels
also: increased glycogenolysis, increased gluconeogenesis, increased mobilization and use of fat
use of NE and epi
cardiac arrest, adjunct to local anesthetic, hypotension, anaphylaxis (epi only), asthma (epi only)
what are the indirect-acting adrenergic receptor agonists? mechanism?
releasers (displace NE from mobile pool): tyramine, amphetamines, and ephedrine
reuptake inhibitors: cocaine and tricyclic antidepressant
drug interaction with adrenergic receptor agonists releasers (tyramine, amphetamines, ephedrine)
MAOa inhibitors - causes HTN crisis when mixed with tyramine (red wine, cheese)
alpha receptor antagonists effects? clinical uses?
decreased TPR, decreased mean BP (normal alpha 1 constriction) - may cause reflex tachycardia and salt/water retention
clinical: HTN, pheochromocytoma, BPH (a1 blocker)
nonselective alpha receptor antagonist drugs? competitive/noncompetitive? clinical uses?
phentolamine - competitive - (acute management HTN)
phenoxybenzamine - noncompetitive (pheochromocytoma)
MAO type A
mainly in liver, but Anywhere (metabolizes NE, 5HT, tyramine)
MAO type B
mainly in brain (metabolizes DA)
what are the selective alpha 1 blockers? clinical use?
prazosin, doxazosin, terazosin, tamsulosin
clinical? HTN and BPH (symptomatic treatment)
what is the selective alpha 2 blocker? clinical use?
what are the beta receptor antagonists?
acebutolol, atenolol, metoprolol, pindolol, propranolol, timolol
which beta receptor antagonists are beta 1 selective?
(A-M) acebutolol, atenolol, metoprolol
which beta blocker causes the least amount of sedation? why?
atenolol - no CNS entry
which beta blockers have no increase in blood lipids? why?
acebutolol, pindolol (because partial agonists)
which beta blocker is best for asthmatics?
which beta blocker is used in social phobias?
uses for beta blockers
angina, HTN, post==MI
labetalol and carvedilol
combined alpha-1 and beta blocking activity - NOT -olol becuase not full beta blockers
what does chronic use of beta blockers lead to?