Adrenergic Blockers Flashcards
Anti-adrenergics
What are the three ways to block adrenergic neurotransmission?
- Decreasing sympathetic outflow from brain
- Suppressing norepinephrine release from presynaptic neurons
- Blocking postsynaptic adrenergic receptors
Two mechanisms that alpha-2 adrenergic receptors inhibit sympathetic neurotransmission
- Postsynaptic receptors inhibit sympathetic neurons that exit the brain
- Presynaptic receptors inhibit NE release
Effect of alpha antagonists on heart
Vasodilation-Increases HR because compensates for postural hypotension
Effect of beta-2 blockers
Increase intraocular pressure and exacerbate asthma symptoms worldwide
Use of beta 2 blockers
NEVER
Competitive antagonists to adrenaline
Tolazoline
Non-competitive/covalent antagonist to adrenaline
Phenoxybenzamine (only for life-threatening)
Adrenoceptor block effect on heart
Prevents increase in HR in response to threats, pacemakers continue regardless (susceptible to disease), must use echo/stress test first!
Adrenoceptor block effect on CV
Decreased PR
Phaeochromocytoma
Endless secretion of catecholamines, treated by alpha adrenoceptor antagonists
Effect of beta adrenoceptor blockers on heart
Increased contraction of the heart demands more oxygen (can’t in CAD–>hypoxemia, necrosis)
Most potent treatment of glaucoma
Timolol
Which is used more, propramolol or atenolol?
Propramolol has greater safety and we know it works, atenolol tests still underway (but may become more common later)
Renin effect on body
More renin in body–>constricted arteries, more fluid in kidneys, more absorbed into circulation instead of released from body