pharmacology 5 - autonomic system Flashcards Preview

cfc - pharmacology > pharmacology 5 - autonomic system > Flashcards

Flashcards in pharmacology 5 - autonomic system Deck (16):

what does the autonomic nervous system consist of? (3)

1, sympathetic division
2. parasympathetic division
3. enteric nervous system.


what does the autonomic nervous system control? examples?

it controls involuntary activities. (non-concious)
eg. CVS, resp, endocrine, Gi tract motility and secretions, repro and urogenital tract.


explain the SNS? where do you find the cell bodies? axons synapse at 3 sites? most commonly?

find cell bodies from 1st thoracic to 3rd lumbar segments.
axons synapse:
-paravertebral (parallel to spine) - most common
-prevertabral (in thorax/abdomen)
-terminal (close to organ)


what are the neourotransmitters for the SNS? what kind of innervation does the SNS have compared to the PNS?

1, preganglionic = ACH at nicotinic receptors
2. norepinephrine (NA) - postganglionic at adrenoreceptors released from the nerve.
3. epinephrine - also postganglionic at adrenreceptors - released from adrenal medulla.

the SNS has a much more diffuse innervation then the PNS.


what could you describe the response of the SNS as? give examples of the actions?

- mydriasis (pupil dilation due to constrivction of the radial mm)
-positively chonotrophic (increased heart rate)
-positively inotrophic (increased force of contraction)
-positively dromotrophic (increased speed on conduction)
- may vasodilate or constrict depending on receptor (mainly constrict) increased peripheral resistance.
reduced GI motility and secretions
-increase urinary sphincter tone (prvent urination)
-glycogenolysis and GNG - increase glucose available - energy!!


what are the characteristic of norepinephrine? precursor? what is the main route of re-uptake etc? what role do alpha adrenorepectors play?

precursor - tyrosine!! also dopamine involved. once made it is stored in nerve terminals until an action potential come along nerve.
it undergoes mainly re-uptake but also enzymatic degratation.
alpha and beta adrenoreceptors.

alpha 2 adrenoreceptor - negative feedback on nerve terminal!!


explain the re-uptake of norepinephrine? 2 enzymes? which more important?

2 enzymes:
-MAO - monamine oxidase - breaks down to release tyrosine in nerve terminal \9\re-used)
-COMT - catechol-o-methyl transferase - into non terminal tissue (not re-used).


What are the SNS receptors? what kind of receptor? which second messanger? what second messanger for each receptor?

they are alpha and beta adrenoreceptors. 1/2.
they are GPCR - 7 transmembrane domains and couple to a second messanger within the cell itself. set up a cascade to release calcium - cell actions.
alpha 1 - coupled to Gq . second messanger is PLC - IP3 - DAG (CA2+ FROM SR) AND PKC which opens up ca2+ channels allowing influx to the cell.
alpha 2 - couple to Gi and Go . inhibit CAMP. which inhibits calcium and activates k+ channels 9RMP more negative.
beta 1 - couple to Gs (stimulate) and cause increased CAMP. and PKA. - increased calcium. cause positive effects on heart.
beta 2 - couple to Gs or Gi. can stimulate or inhibit CAMP. cause vascular sm relax (increased CAMP) bronchddilate, stabilise resp mast cells (asthma)


explain alpha 1 adrenoreceptor action when NA binds? actions? second messanger?

coupled to Gq receptor. causes PLC - cascade - DAG, IP3. PKC, SR - CA2+!!!
causes vasoconstriction
positive on heart
stimukate and contract prostatic sm
increase peripheral resistance
urinary sphincter contract
mydriasis (dilate pupil?)


alpha 2 adrenoreceptors? properties? what do they mediate? if lowered camp what happens to vascular sm?

coupled to Gi and Go. inhibit CAMP! less ca2+ release. activate k+ channels so moves out of cell and hyperpolarised. less likely to fire AP. inhibit neurotransmitter relase to (negative feedback) cause vasoconstriction (less cAMP) mediate sedation and analgesia!! i
if myocardial CAMP - down = relax
up = contract.


beta 1 adreoreceptors. coupled to?

coupled to Gs. (stimulate) heart. increase CAMP. inotrophic, chonotrophic, dronotrophic


beta 2 adrenoreceptors? mediate to which receptor? can do either? good for what type of disease?

Gs and Gi. can inhibit or stimulate via CAMP. vasculr SM relaxation (increased camp) Gs.
stabilise mast cells resp - less likely to release histamine - asthma (b2 agonists)


PNS - outflow from where? synapse where? neurotransmittier? receptors?

craniosacral outflow! - ACH neurotransmittir. synapse near organs (much more localised effect than SNS) nicotinic receptors and presynaptic and muscarinic receptors are postsynaptic.


how is ACH removed from nerve terminal? precursor? what is CAT?

mainly enzymatic degradation. AChetylcholine esterase. choline precursor is taken back up and used again. CAT - choline acetyl transferase - synthesis of ACH.


How can you explain action of PNS? give examples of the actions of the PNS? CVS? gi tract? urinary? eye? resp?


CVS - decreased heart stuff
vasodilation and induces NO release (causes vasodilation)

GI tract - increased motility and secretions.
Urinary tract - contract detrusor, urethral peristalsis, relax sphincters
Miosis - pupil constriction
Respiratory - bronchconstrict and less secretions.


PNS receptors? 2 nicotinic? 5 muscarinic? M2 DOES WHAT?

nicotinic - presynaptic (common with SNS) ligand gated ion channel. increases permeability to NA and K+ .
Nm and Nn.
Nm - skeltal muscle (somatic NS)
Nn - ganglia 9autonomic)

Muscarinic - postsynaptic.
GPCR's. M1-M5.
even - negative on CAMP. open k+channel
odd - PLC coupled and increase CA2+.