4 - autonomic Flashcards
what do α1 receptors do to blood vessels (3 things)
vasoconstriction, increase arteriolar resistance, increase BP
what do β receptors do to blood vessels (4 things)
smooth muscle relaxation, vasodilation, decreased peripheral resistance, decrease BP
what kind of receptors are on skin and spleen vessels
why is this advantageous
α1
when NA activation (sympathetic), you dont need blood to those unimportant internal organs
what kind of receptors are on muscle blood vessels
why is this advantageous
β2 and α1
will constrict/dilate depending on which receptors are activated
what do α2 receptors do to NA release and why
they decrease NA release because they are autoreceptors
what do β receptors do to NA release
increase
what happens with low NA at a nerve terminal with β and α2 receptors
you will get more adrenaline because α receptors are less sensitive than β, so the β effect is predominant
what happens with high NA at a nerve terminal with β and α2 receptors
less NA because α are less sensitive but they can turn it off at high amounts
what kind of adrenoreceptors are found the most in the heart
β1
what do β1 receptors do in the heart (4)
increase Ca++ influx, increase force and rate of contraction, increase conduction of the AV node
why can β agonists be dangerous for heart
because of severe cardiac dysthythmias (heart contracts out of sequence due to excessive Ca2+ influx)
what kind of receptors does phenylephrine target
pure α
what do pure α agonists do to BP and HR? give an example.
increase peripheral resistance and decrease venous capacitance (willingness to change size). phenylephrine
BP increases - so HR decreases due to baroreceptor reflex
what kind of receptors does isoproterenol target
pure β
what do pure β agonists do to body (cardio)
increases cardiac output (β1) and decreases peripheral resistance(β2)
what happens do BP and HR with β agonists
fall in BP (β2 in skeletal muscle)
increase in HR (β1 in heart)
what receptors does adrenaline stimulate
α and β
what does adrenaline do to the body
HR increase (β1), vasoconstriction (α) then later BP falls because β2 become selectivly stimulated (β is more sensitive to NA, so its vasodilatory effects with prevail)
what would happen clinically (symptoms) with an increase in blood pressure
severe headache
what would happen clinically (symptoms) with an decrease in blood pressure
syncope (fainting)
what do α agonists do to eye
mydriasis as the radial pupil dilator muscle of iris is stimulated
what do β agonists do to the lungs
β2 stimulation relaxes bronchiole smooth muscle
where are α agonists do in the nose
nasal blood vessels constrict, reducing congestion
how do α2 agonists affect the gastrointestinal tract
indirectly relaxation by inhibiting the release of ACh, since alpha receptors are present on ACh releasing neurons
what β2 agonists do to the gastrointestinal tract
relaxation
what do α receptors do to genitourinary tract
constrict bladder base and internal sphincter - cant pee
what does α2 do to endocrine function
inhibition of insulin and renin
what does β2 do to endocrine function
release insuline and renin
what does β activation to do metabolism (2)
β3 lipolysis in fat cells
β in liver promote glycogenolysis
what drugs pass the blood brain barrier the easier
ones that are neutral
what can happen with drugs that easily pass the BBB
nervousness, anxiety
what are the effects of amphetamines
mild alertedness, improved attention, elevate mood, insomnia, euphoria, anorexia (involves dopaminergic mechanisms)
what is a therapeutic use of adrenaline in anesthesia
after being mixed with local anesthetics, it can help prevent loss of anesthetic into systemic circulation (it is vasoconstrictive) so it lasts longer
how does adrenaline help with anaphylaxis
causes the opposite effect of the allergic reaction from histamine (bronchospasm, mucous release, membrane congestion, angioedema, BP drop)
what receptors does isoproterenol activate and what does it cause
β1 cardiac stimulant
β2 vasodilator
what can isoproterenol be used for clinically
cardiac arrest or AV block (beta 1 agonism)
good for hypertension (beta 2 agonism)
what is the cheese effect of tyramine
if people are on MAO inhibitors, tyramine won’t be broken down by MAO in the liver, pharmacologically induces catecholamine release, which causes hypertension and cardiac dysrhythmia
what does cocaine do to NA and DA
inhibits reuptake 1 into neuron terminal
what are the mental side effects of cocaine
alert, mood elevation, insomnia, euphoria
what causes the euphoria from cocaine
central catecholamines, like DA
what can be a therapeutic use of cocaine
in surgery as a local anesthetic (also good cause its a vasoconstrictor so then the drug wont leave and cause euphoria)
what is methylphenidate
ritain, an amphetamine
what do amphetamines do to CNS
alert, elevate mood, insomnia, euphoria, anorexia
what are 3 therapeutic uses for amphetamines
ADHD, narcolepsy, diet pills
what do amphetamines do to DA and NA
enter the presynaptic terminal to releases DA/NE from vesicle IN THE ABSENCE OF ACTION POTENTIALS
also runs the transporter in reverse, increases monoamine release
what is dobutamine
β1 cardiac stimulant (NO beta 2 effect)
what is the theraputic role of dobutamine
emergency for acute heart failure or cardiogenic shock (NO BETA 2 effect)
what is salbutamol and what is it used for?
β2 selective bronchodilator
used for asthma
what is phenylephrine
α agonist, (α1), vasoconstrictor, long lasting, not metabolized by COMT
what is a therapeutic use for phenylephrine
nasal decongestion, constriction of blood vessels to mucous glands (since it is a alpha 1 agonist)
how can optometrosts cause mydriasis
α agonist like phenylephrine (dilate the eye)
what do α antagonists to do BP and peripheral resistance
lower peripheral resistance and blood pressure (blocking sympathetic tone)
what are some negative reflexes of α antagonists
postural (orthostatic) hypotension, reflex tachycardia (Fast)
how can optometrists do miosis
block α
block sympathetic constriction of iris radial muscle
what can α blockers do to the nose
cause stuffiness (dilate blood vessels supplying mucous glands)
what is phentolamine
α1 and α2 blocker used to lower BP and promote tachycardia
what does phentolamine do to BP
lowers because of α1 blockage
what does phentolamine do to HR and how
increases it due to
- baroreceptor reflex
- increase NA release onto unblocked β receptors AND blockade of α2 receptors
what does phentolamine do to α2 receptors
blocks them so that there is no negative feedback loop to regulate NA release - causes tachycardia
when can you use phentolamine therapeutically
with adrenal medullary tumors that release large quantities of catacholamines
what receptors does prazosin target
α1 antagonist - highly selective
what does prazosin do to body
relaxes arteriolar and venous smooth muslce sinze it is an alpha 1 sympathetic antagonist
why does prazosin make less reflex tachycardia than phentolamine
prazosin does not inhibit α2 (which are involved in negative feedback regulation of NA) since it is specific for alpha 1 antagonism
what condition can prazosin help with
prostate issues/ urinary obstruction
what receptors does propranalol target
antagonist for β 1 and 2
what are 6 therapeutic uses of propranolol
hypertension prophylaxis of angina pectoris heart failure cardiac dysrhythmias hyperthyroidism anxiety
how does propranolol help with hyperthyroidism
excess thyroxine stimulates the sympathetic system, so this helps reduce the sympathetic response since it is a beta 1 and 2 antagonist
what effects do β blockers have when at rest
not a ton because the heart is under parasympathetic tone-needs sympathetic stimulie
what do β blockers do to the body during exercise (3)
may decrease HR, AV conduction and contractile response
what does acute use of β blockers have on blood pressure
acutely may increase BP following block of peripheral BP receptors since the alpha 1 receptors will dominate
what what does chronic use of β blockers do to body
1-alteration of central sympathetic outflow (reduce)
2-decreased renin release!
3-blockage of presynaptic B receptors
what does blockage of presynaptic B receptors do
decreases NA release (B autoreceptors increase NA release-positive feedback)
what do presynpatic α2 receptors do
inhibit NA release
what do presynaptic β receptors do
increase NA release (positive feedback)
why can you get rebound hypertension when you stop taking β blockers
decreased NA outflow causes upregulation in postsynaptic α adrenoceptors
-so when β blocker is removed, NA release is normal and there are so many more α receptors to receive the NA - HYPERTENSION
what does blockage of β2 receptors do
increase airway resistance (constrict bronchioles)
what are some weird β blocker ways of stimulating receptors (2)
partial agonist (only partly stimulate receptor) inverse agonist (opposite of blocking β receptors)
what receptors does Metoprolol get
β1 selective
what kind of diseased people benefit from metoprolol instead of propranolol
asthmatics, diabetes and patients with peripheral vascular disease (β2 still works in vessels)
