Flashcards in Autonomic Pharm Deck (102):
NEpi has activity on the heart, if stimulated the clinical effect is?
What is NE effect on blood vessels?
Constriction leading to higher BP
Sympathetic N.S. describe
Fight or flight. Involved with exercise, activation, arousal
Rest and digest, recovery.
2 systems of ANS
Sympathetic and Parasympathetic
NT has to be synthesized where?
In the cell
Name the 3 main 2nd messenger systems
1. Phospholipase C
2. Adenylyl Cyclase
3. Guanylyl Cyclase
What do 2nd messenger systems do?
They get signal across so stimulation can occur. They are triggered when NT hits receptor, they are bystanders. They do the grunt work. They do all the work and help signal transmission
Are 2nd messengers intra or extracellular?
Which is not a 2nd messenger system?
1. Guanylyl cyclase
2. Phenyl A esterase
3. Adenylyl cyclase
4. Phospholipase C
Phenyl A esterase (made up)
This drug is given in emergency and is an anti chollenergic. It works specifically on M2 (muscarinic 2) So when it is given it blocks M2 to decrease HR.
Drugs that bind directly to muscarinic receptor are called?
______ bind to the muscarinic or nicotinic receptors resulting in activation
Direct binding agents
______inhibit AChE(E is for estherase), therefore resulting in an increase of Ach in the synaptic cleft
Indirect acting agents
_____is an enzyme designed to break down Ach so if you prevent breakdown you _____ amount cause there is no where to go
If more Ach at receptor it should cause _______ but if you prevent it from being broken down that should cause more _______ too b/c it should be broken down and recycled and whole process started over again
More activation, more activation
m1-m5 all activated by what?
Drug that is specific for N(m) for example _____ Ach and ____ muscle movement
Which muscarinic receptor is directly innervated with the myocardium?
What are the 5 steps in synaptic transmission? (test)
1. Transmitter synthesis
2. Transmitter storage
3. Transmitter release
4. Receptor binding
5. Termination of transmission
NT dissociates from receptor and is removed from synaptic gap by: (3 ways)
1. Reuptake (recycled)
2. Enzymatic degradation (got digested by another enzyme system)
3. Diffusion (goes from high concentration to low)
If depleted NT being made (synthesized) then impact on receptor is ________
What happens if binding to receptor is blocked? (test)
Shouldn't be activated as much if blocked, so decreased
Inhibiting neurotransmitter release from presynaptic nerve terminal will ____ receptor activation (test)
Block or decrease. (simple concept, if you have more, you have more activation. if you have less, then you have less activation)
Increased synthesis of neurotransmitters will ______ receptor activation
Inhibiting neurotransmitter breakdown will ______ receptor activation
increase (example: if sitting there at end of receptor but prevent it from being broken down and starting process over it should increase the activation which makes sense cause can't reset whole cycle and start over if its still sitting there).
_____ mediates responses at cholinergic receptors
Acetylcholine (Ach) "CH"
_____ mediates responses at adrenergic receptors
Norepinephrine (NE) "NE" or Epinephrine (similar to NE)
_____ mediates responses at dopaminergic receptors
Adrenergic receptors have 5 subtypes, what are they?
Alpha(1) Alpha (2) Beta (1) Beta (2) Dopamine (DA)
If Ach is blocked you will have a ____ activity on these receptors ______
decreased, nicotinic n, nicotinic m and muscarinic
Receptor is specific to the ______ they are one in the same
Epinephrine is released and activates b1 receptor, beta 1 receptor is on the heart, what is the clinical outcome? (test)
Increased stimulation, heart rate increases
X vagus nerve acts on what?
Heart, GI tract
Ach is produced in neuron from ______
Acetyl-CoA synthesis occurs in the _____
Ach storage and release phenomena can occur at a ______
very fast speed. Storage and release are mili seconds. Enzyme system is quick at digesting and starting process over again.
When Ach is activated on vagus nerve is can ______ HR
decrease. direct stimulation=decrease heart rate
Fancy term means vesicles got to end of neuron and opened up
What is eliminated by enzymatic hydrolysis via AchE?
Ach, its the main way it's degraded
What causes a versicle to open up?
change in charge causes vesicle to open and NE is released then goes to receptor to bind
_____ is an enzyme responsible for breaking down catecholamines, one of those responsible for breaking it down and recycling the whole process
MAO-Mono amene oxidase
What is a catecholamine?
Included among catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine.
Catecholamine release is triggered by?
Action potential or charge
Action potential results in influx of ____ in the nerve terminal and fusion of granules resulting in _____ of NE
enzyme system outside the neuron responsible for degradation of NE is ______(test)
MAO is __________
Enzyme system inside responsible for degrading NE is _______(test)
What is NET?
Norepinephrine transporter. basically is reuptake back into neuron.
What is an agonist?
An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response.
What is an antagonist?
A receptor antagonist is a type of receptor drug that blocks or dampens a biological response by binding to and blocking a receptor rather than activating it like an agonist.
What is an anticholinesterase?
Drug that prevents Ach metabolism, maintain ach concentration at each effector site ach is released. It's a drug that blocks AchE. Drugs that block acetylcholinesterase (achE)
AchE does what?
breaks down Ach
A way to increase Ach activity is to give an ______, can give these after surgery to restore muscle function
Main anticholinesterase given at controlled dose that is most effective at restoring neuromuscular function after a blockade?
Neostigmine-has direct and indirect action
____ blocks Ach
Atropine (atropine is antichollenegic)
If Ach is blocked @ the muscarine receptor of the heart what should be the clinical effect be? (test)
Answer: increase HR
(Stimulation causes decrease HR)
The neuromuscular system Nm when its activated with Ach it should cause ______
contraction of skeletal muscle
If muscarinic receptors in the lung m3, if stimulated should cause ______
broncoconstriciton and increase flow of secretions
When Ach is activated on muscarinic receptor in heart stimulation translates to __________
decrease HR, bradycardia
Epinephrine works on what receptors?
a1, a2, b1, b2
Norepinephrine works on what receptors?
Dopamine works on what receptors?
Alpha 1 when activated does what?
Vasoconstriction, leading to increase BP
________ is a direct adrenergic agonist
Couple examples that block NE reuptake _____
Cocaine, tricyclic antidepressants
What's the difference on B2 activity of Epi vs NE? (test)
A: NE has none, epi should cause bronchodilation
Albuterol is b2 agonist so when inhaled it activates _____receptors and b2 causes _______
activates b2 receptors, and b2 causes bronchodilation or opening of the lungs
a1 receptor location?
eye, peripheral vasculature (prodominatly concentrated in arteries and veins)
a2 receptor location?
CNS, peripheral vasculature
Skeletal muscle, lungs, uterus, liver (know cardiac related)
Domapine is in the _____
Name 3 endogenous catecholamines (endogenous means in body)
NE, EPI, DA. Catecholamines directly stimulate adrenergic receptors and activate effector tissues
_____ is mainly in adrenal medulla
______ is mainly in sympathetic nerve endings
a1 stimulation causes ______
Mydriasis, widening of the pupil.
If a1 is stimulated on blood vessels they should _____ and the clinical outcome is______
constrict, increased blood pressure
a2 decreases release of ____ (exception to the rule)
b1 is predominately on the _______ , also related to renin release on _____
Increases HR and increase force of contraction (main effects of b1 stimulation)
b2 when stimulated _______ up airways in lungs.
opens up airways. Albuterol is b2 agonist, its effects on the lungs are to dilate so patient can breathe better
In blood vessels b2 ______ vessels
dilates for increased blood flow
A b1 agonist will do what on the heart?
Increase HR and force of contration
Epi and NE when they act on a1 should ______ the veins so it translates to ____ BP
constrict, increased BP
If a1 antagonist what affect would that have on the blood vessels and what affect on bp?
Dilates and lowers BP. Also causes constriction of pupil.
Stimulating a1 receptor would cause what in eye?
Eye-Contraction of radial muscle of iris (mydriasis)
Stimulating a1 receptor in arterioles would do what?
skin, viscera, mucous membranes, veins. Stimulating a1 in sex organ=ej
Stimulation of a2 receptors located in presynaptic nerve terminals does what?
Inhibition of transmitter release
Stimulation of b1 receptor in heart does what?
Increased rate, increased force of contraction, increased conduction velocity
Stimulation of b1 receptor in kidney does what?
Stimulation of b2 in arterioles does what?
Dilation. Heart, lungs, skeletal muscle.
Stimulation of b2 in bronchi causes what?
Dilation, increased breathing
Stimulation of dopamine in kidney does what?
dilation of kidney vasculature
Miosis is what?
Pupil constriction muscarinic stimulation
Midriasis is what?
Pupil dialtion a1 receptor stimulation
Nicotinic N is located where and what does stimulation do?
Located: All ANS nervous system ganglia
Stimulation: Of nerves causes Epi release from adrenals
Nicotinic M are located where and what does stimulation do?
Located: Neuromuscular junctions
Stimulation: contraction of skeletal muscle
Stimulation of muscarinic in the eye causes what?
Contraction of ciliary, leading to miosis "constriction" decreased pupil diameter
Stimulation of muscarinic receptor in heart does what?
Stimulation of muscarinic receptor in lung does what?
Constriction of bronchi & promotes secretion
Stimulation of mucarinic receptor in bladder does what?