Pharmacology - autonomic Flashcards
t/f sympathetic preganglionic neurones are ACh
true
post - usually noradrenaline
4 cranial parasympathetic nerves
3,7,9,10
for neurochemical transmission, the first 4 steps are
precursor taken up
transmitter synthesised and stored
action potential depolarises
calcium influx through voltage-activated channels
what does this lead to 3
calcium induced release of transmitter
activates receptor
enzyme-mediated inactivation/reuptake of transmitter
chemical transmission for sympathetic system initiated by release of ACh, how is this done (2)
action potential from cns reached
travels to presynaptic terminal, triggers calcium entry and releases ACh
ACh opens ligand-gated ion channels in the postganglioinic neurone, what does this cause
calcium is able to enter and release noradrenaline
what type of receptor does noradrenaline activate
G-protein coupled receptors (adrenoceptors)
what are the receptors in target cell membranes that are activated by ACh in parasympathetic chemical transmission
muscarinic acetylcholine
strucure of ligand-gated ion channels, what do they do, what does this cause
several glycoprotein subunits - channel
rapid changes in permeability of membrane to certain ions (Ca,K)
rapidly changes membrane potential, allows action potential to be reached and transmission of neurones
G-protein coupled receptors can be broken down to the receptor and protein constituents, outline strucutre of each
receptor - integral membrane protein
-7 transmembrane spans - joined by 3extrac,3intrac loops
G-protein - 3polypeptide subunits (alpha,beta gamma)
- alpha = binding site of GDP/GT
P
prior signal, GPTR’s have GDP binded, no receptor occupied, and so no effector modulatioin. WHat happens when the signal is turned on (6)
agonist activates receptor
Gprotein couples with receptor
GDP dissociates,
GTP binds to alpha
Gprotein dissociates (beta,gamma)
alpha binds to effector
agonist dissociates
t/f after agonist dissociates, signalling can persist
true
how is the signal of a GPTR turned off
alpha subunit hydrolyses GTP - GDP
alpha recombines with rest of Gprotein (beta,gamma)
what type of receptor are nicotinic acetylcholine receptors? structure
ligand-gated
5 glycoproteins
lots of subunits
cholinergic transmission is for what neurotransmitter
acetylcholine
outline cholinergic transmission
uptake of choline ACh synthesised and stored Depolarisation - calcium influx, releases ACh ACh receptors activated ACh degraded via reuptake
what terminates cholinergic transmission
AChE
examples of agonist for ACh
nicotine
at parasympathetic neuroeffector junctions,name of receptors activated
Muscarinic ACh receptors 1-3
what is ACh degraded to
Choline
Acetate
Muscarinic ACh receptors at parasympathetic neuroeffector junctions are g proteins, what is the function/effect of each
M1 - stimulates phospholipase C - incr stomach acid secretion
M2- inhibits adenylyl cyclase, opening of K+ channels, decr HR
M3 - stimulates phospholipase C , incr saliva secretion and bronchoconstriction
what two enzymes metabolise noradrenaline
MAO
COMT
`Noradrenergc transmission through B1,B2,A1,A2
B1 - inhibition of adenylyl cyclase - incr HR and force
B2- stimulation adenylyl cyclase - relaxation of bronchial and vascular smooth muscle
A1 - stimulation of phospholipase C, smooth muscle contraction
A2 - inhibition of adenylyl cyclase - inhibits NA release
prazosin is a selective antagonist of A1, explain effect and when used
vasodilation
antihypertensive
drug which is a competitive antagonist for B1, what is it used for
Atenolol (beta-blocker)
antianginal, antihypertensive
salbutamol is an agonist for
B2
t/f atropine is competitive antagonist of nicotonic ACh receptors, yet does not block muscarinic ACh receptors
false
antagonist for muscarinic, not nicotonic
effect of atropine , when is it used
blocks parasympathetic activity
post MI bradycardia
AChE poisoning
