Adrenergic Antagonists Flashcards
nonselective antagonism of ALPHA receptors is useful in treating ?
phaeochromocytoma
alpha 1 selective antagonists treat ? and ?
Htn
BPH
most common adrenergic antagonists used?
beta antagonists
*Htn, ischemic heart disease, arrhythmias, endocrinologic, neurologic disorders
phentolamine
phenoxybenzamine
non selective alpha 1 antagonists
phenoxybenzamine is slightly alpha 1
only alpha 2 selective?
yohimbine
alpha 1 selective?
prazosin
doxazosin
terazosin
tamsulosin
reversible nonselective alpha? irreversible?
phentolamine
phenoxybenzamine
irreversible will shift the curve to higher concentrations (also reversible) AND it will ?
reduce the maximum effect
blockade of alpha receptors in smooth m reduces ? and ?
peripheral resistance
blood pressure
giving an alpha antagonist to a mixed a&b agonist i.e. epi would result in?
known as??
fall in peripheral resistance (NO EFFECT ON B)
fall in BP (antagonizes alpha)
EPINEPHRINE REVERSAL
giving an alpha antagonist to NE?
just blocks the increase in BP
practically no B receptor activity w/ NE
on the heart, alpha antagonists do two things:
- decreased blood pressure leads to reflex tachycardia via B1 receptors
- presynaptic a2 receptors that decrease NE release are blocked, increasing NE release on heart & increasing HR and force of contraction
blockade of a1 receptors in VEINS can results in ?
orthostatic hypotension
phentolamine used in treatment of ? and ?
|»_space;causes a drop in ? thru inhibiting a1 and reflex stim of ? to the heart (tachycardia)
hypertension
pheochromocytoma
peripheral resistance
SNS nerve terminals
presynaptic inhibition of a2 causes an increased release of ? from sympathetic nerve terminals and an ? of reflex tachycardia
exacerbation
- net result is vasodilatation, increased CO&rate
- little effect on BP of patients with essential hypertension
phentolamine ALSO inhibits ? receptors and activates ? and ? receptors
dopamine
muscarinic, histaminergic
*adverse effects include severe tachycardia, arrhythmias, myocardial ischemia, nasal congestion, and headache
phenoxybenzamine inhibits ?, histamine, Ach, and serotonin receptors
-can cause ? from the presynaptic a2 blockade
NE reuptake
reflex tachycardia
*treatments same as phentolamine- Htn, phaeochromocytoma
A/E of phentolamine and phenoxybenzamine include tachycardia, postural ?, nasal stuffiness, sexual ?, fatigue, sedation, and nausea
hypotension, dysfunction
Tx for raynaud’s syndrome?
*also relieve Sx in ? and useful in ?
prazosin*, terazosin, doxazosin
BPH, BPH w/ comorbid Htn
alpha 1 selective adr ant have less ? due to its lack of ?
reflex tachycardia, a2
alpha one selective
3 hours?
9-12 hours?
22 hours?
praZOSIN
teraZOSIN
doxaZOSIN
4th a1 selective but structurally diff?
-met in the ?
higher potency for inhibiting ? contraction but less potency at vascular smooth m compared to other three
-used for relieving ? while producing less ?
tamsuLOSIN
liver
urinary retention in BPH
BPH, hypotension (use other in hypertensive pts)
a2 selective adrenoceptor antagonist?
-? effect that produces increases in HR, BP, anxiety and agitation
yohimbine
antidiuretic
**more serious a/e have been reported including renal failure, seizures, death
partial agonists that are also beta blockers? (2)
- inhibit activation of B receptors in presence of ? but moderately activate receptors in presence of ?
- said to have?
pindolol, acebutolol
high catecholamine concentrations
endogenous agonists
block alpha and beta receptors?
carvedilol, labetalol
in normotensive patients, taking beta antagonists does not usually cause ?
hypotension
at rest the PNS innervation of heart dominates» therefore blockade of B receptors would ?
have little effect
Propanolol
- decreased CO results in a transient reduction in ? activating a baroreflex increase in SNS outflow
- ? will increase due to ? (normally vasodilatory)
- the reflex increase in SNS outflow and less B2 receptor mediated vasodilation combine to increase the ? on vascular resistance causing an increase in ?
blood pressure
peripheral resistance, blockade of B2 receptors
SNS, arterial pressure
B1 selective agents will not block B2 vasodilation so there will be less of a decrease in ?
diastolic pressure
CHRONIC USE of B blockers:
- in presence of ? total peripheral resistance returns to ? or is ?
- delayed fall in ? and persistent reduction of ? accounts for its ? actions
- beta blockers also reduce the release of ? from the kidney
hypertension, initial value, decreased
peripheral resistance, CO, antihypertensive
renin
drugs used to treat supraventricular arrhythmias and ventricular arrhythmias?
beta blockers
**also useful in angina, MI, and HF (the HF is counterintuitive because the heart is failing/decreased CO)
due NOT give an asthma patient a B2 blocker ie?
propanolol
*EVEN B1 selective agents at a high enough concentration can antagonize B2 receptors
mixed acting agents like ? hold promise in patients w/ asthma
celiprolol
nonselective B ant and B2 ant are CI in ? due to its blockage of glycogenolysis and gluconeogenesis
-B blockers also mask the ? associated with ?, which is a warning sign in diabetics
insulin independent diabetes
tachycardia
hypoglycemia
chronic use of B blockers is associated with an increase in ? and decreased ? which is undesirable in CVD; also increases risk of CAD
VDL, HDL
b blocker used to decrease IOP in GLC? used in conjunction with muscarinic agonist?
timolol
pilocarpine
labetolol
penbutolol
pindolol
acebutolol
partial agonists
longest acting beta blocker?
nadolol
alpha 1, beta 1 and partial agonist B2; can cause orthostatic hypotension
labetalol
ultra short B-1 selective?
esmolol
b1 selective widely used, htn, angina, MI
metoprolol
most b1 selectivity, NO mediated vasodilation, hypertension
nebivolol
to reduce effects like fatigue, sedation, sleep disturbances, depression, etc. use agents with lower ? like ? or ?
lower lipid solubility
nadolol, atenolol
B1 selective agents should only be used when completely necessary because they still ?
acting on the b2 receptor (asthma- bronchoconstriction)
life threatening a/e from b-blockers - being used in CHF or MI- reverse with ? or ?
isoproterenol
glucagon
b-blockers can interact with the ca2+ channel antagonist ? and cause bradycardia, HF, severe hypotension
verapamil
insulin dependent diabetes- give a ?
b1 selective blocker (as little activity on b2 as possible bc that deals with liver glycogenolysis&gluconeogenesis)
men complain of ? from b-blockers
impaired sexual activity
guanethidine
metyrosine
reserpine
indirect adrenergic; nonselective!
blocks the synthesis or release of catecholamines
blocks release of NE & can displace NE from storage vesicles?
guanethidine
inhibits tyrosine hydroxylase and prevents catecholamine synthesis?
metyrosine; rarely used to reduce pheochromocytoma
blocks uptake of catecholamines from cytoplasm to vesicles? results in accumulation of NE in cytoplasm degraded by MAO, decreasing BP and HR
reserpine
*long-acting and effects persist for days
