Excitation-contraction Coupling Flashcards
Which nerve parasympatheticaly innervates the heart?
where on the heart does it innervate?
What effect does it have on heart?
- VAGUS 10th Cranial nerve
- synapses with SA and AV node
- post ganglionic cells release Ach
- acts on M2 receptors
DECREASE Heart Rate
DECREASE AV node conduction velocity
describe how the resting membrane potential of cardiac cells is
generated
- K+ PERMEBAILITY SETS THE RMP*
- cardiac myocytes r more permeable to K
- K+ ions leave the cell down their concentration gradient
- this makes the inside negative
- as charge builds up an electrical gradient is made.
draw the changes in membrane potential and describe the ionic currents underlying the cell AP of
(i) ventricular cells
(ii) pacemaker cells
P
describe the processes of excitation - contraction coupling in ventricular myocardial cells.
P
describe the factors influencing the changes in intracellular free Ca + concentration of ventricular cells during the AP
O
explain the effects of hyper and hypokalaemia on the heart
hyper > Increased extracellular K levels result in depolarization of the membrane potentials of cells, due to the increase in the Ek. This depolarization opens some voltage-gated sodium channels, but also INACTIVATES them at the same time.»_space;SLOWER DEPOLARISATION UPSTROKE
Hypo > delays repolarization
LENGTHENS AP
describe the membrane potential changes in pacemaker cells associated with increases and decreases in heart rate.
P
detail the neurotransmitters and receptors involved in the
autonomic nervous system
O
explain the cellular mechanisms by which the autonomic nervous system controls
1) heart rate
2) force of contraction in the normal heart
O
describe the mechanisms which control contraction of vascular smooth muscle cells
O
explain the role of the ANS in controlling peripheral resistance
P
what r pacemaker cells?
specialised cells that generate an electrical event at regular intervals.
the AP
distinguish btw AP in Pacemaker cells & ventricular myocardial cells
,
what structure conducts excitation through the ventricular myocardiam?
purkunjee fibers
why is the cardiac AP much longer?
bc of the ‘plateu phase’ caused mainly by calcium
describe how RMP is made
- K+ PERMEBAILITY SETS THE RMP*
- cardiac myocytes r more permeable to K
- K+ ions leave the cell down their concentration gradient
- this makes the inside negative
- as charge builds up an electrical gradient is made.
what channel is responsible for the upstroke of the AP in pacemaker cells?
L-type Ca channels!
*
*AT AN EQAULAIBREM OF AN ION, THE CONCENTRATION GRADIENT AND ELECTRICAL GRADIENT R THE SAME
reminder
describe what happens during platue phase
voltage-gated ca+ channels (L-type)»_space;ca+ influx
FEW K channels»_space; efflux
this balances the potential
what is the pacemaker potential?
refers to a LONG SLOW depolarization to threshold, its due to a ‘funny current’ which r made by channels called HCN
In SA and AV node
what is meant by the “funny current?” what channels r responsible for it
during pacemaker potential, it spontaneously depolarises from its most negative value (-60mv) due to HCN channels (open due to hyper polarisation). this initial depolarisation is known as the funny current
draw the SA node action potential, what shape does the graph give?
- LONG depolarisation to threshold via HCN
- upstroke via L-type voltage gated ca channels
- downstroke opening of voltage-K channels
what is a special feature about the SA node AP
they don’t ever sit at rest, they spontaneously depolarise, they don’t need neighbouring cells to activate them (3ala kayf umhum)
what channels make the funny current?
HCN channels, influx of Na+ channels (SLOW sodium channels)
special features of voltage channels
they activate as well as inactivates
what is the difference btw the Na channels in pacemaker & and ventricular myocyte
Na+ channels in the pacemaker r HCN slow Na channels that make the funny current
Na+ channels in the ventricles r voltage-gated & r responsible for the upstroke depolarisation.
what do HCN channels stand for? what do they do
Hyperpolarisation-activated Cylcic Nucleotide-gated channels.
allow INFLUX of Na channels which depolarises cell to threshold
why is the AV node delayed?
to allow atria to finish contraction
which has a higher conducting velocity, purkunjee or SA/AV node? why?
purkunjee, bc their cells r wider > less resistence, less cells involved and less membranes to cross, has FAST na channels which help in fast conduction.
BUT its depolarisation is slow than SA
if AP failed to occur we have________
asystole
what is normal K value in the blood|?
3.5-5.5 mmol/L
values for hyperkalameia, hypokalmeia
hypokalmeia»_space;»less than 3.5
hyperkalameia»»more than 5.5
why r cardiac myoctyes so sensitive to changes in K+ levels?
bc their RMP is very close to the K equilibrium potential (Ek).
so any change in Ek, will effect the RMP
and they’ve got a lot of Potassium channels!
risks of hyperkalemia and treatment and why
- asystole > heart can stop> bc ur slowing conduction down (wayid ur inactivating na channels)
- increase in excitability
TREATMENT
- Ca gluconate> makes heart less excitable
- Insulin & glucose> insulin promotes K to move into cells
- b2 agonist > pushes K inside
stages of hyperkalmeia
mild > 5.5-5.9 mmol/L
moderate> 6.0-6.4 mmol/L
Severe> 6.5 & more
a patient wants to undergo an open heart surgery, what do we give him to temporarily stop the heart from pumping?
cardioplegic solution :
-high K solution used to bring the heart to asystole or heart paralysis.
why in hypokalemia, is it dangerous that the AP in longer?
u leave it more prone to arrhythmias forming
leads to oscillations in MP > leading to ventricular fibrillation> Less CO
excitation-contraction coupling & different receptors involved
- depolarisation opens L-type Ca channels
- this ca will stimulate CICR channels (RyR) in the SR (theres a close link btw these 2 channels
receptor involved in exitation-contraction
CICR
RyR
L-type volatage Ca channels
describe regulation of cardiac myocyte contraction
hint: start with troponin
ca binds to troponin C
conformation change moves tropomyosin away from actin’s binding site
‘site exposed’
myosin head can now bind to actin
during excitation contraction coupling, where did most of the calcium come from? how r these calciums taken back to normal levels again
SR STORES!!
pumped back in via SERCA
which artery has the thickest smooth muscle wall?
arterioles
excitation contraction coupling in vascular SMC and its regulation
2 ways :
via VGCC
via Gq recepters. (via a-adrenorecepter)
Ca+ comes in, binds with calmodulin, activates MLCK (myosin high chain kinase) which will phosphorylate the myosin light chain to allow interaction with actin.
DAG> PKC> MLCP> will dephosphorylate the myosin light chain leaving it inactive.
look at lecture for detailed pathways
**Troponin C doesn’t have a role in SMC, what r ca bound to then?
CaM»_space; calmodulin
The cardiac action potential is very long, so over most of the heart a single action potential will produce a sustained contraction of the cell lasting about__________ms
200-300ms
- If action potentials fire too slowly →
- If action potentials fail →
- If action potentials fire too quickly →
- If electrical activity becomes random →
bradycardia
asystole
Tachycardia
fibrillation
what happens to all the calciums when its time for the cardiac myocytes to relax?
ca must return back to its resting levels
- most pumped back in SR via (SERCA)
- some exit across cell membrane via Ca Atpase & na/ca exchanger
in which layer is most smooth muscle found?
tunica intima
media
adventita
Tunica media
