control of cardiac muscle Flashcards
what is the heart also knowns as
myogenic
what are the two different action potentials controlled heart rate
pacemaker potential (SAN) atrial/ventricular potential
whats modulation of both these action potentials by
the ANS
where are the SAN located
wall of the right atrium
what are the firing rate of APs
usually 1/s
what does the firing rate of APs equal
the resting heart rate (60-80bp)
what happens to electrical activity when it reaches the AVN
it slows down
what type of resting membrane potentials do SA node cells have
unstable/non-equilibrium resting membrane potentials
what is the RNP of SA node cells
-60mv (slightly higher than normal)
what is the If channel and what is it activated by
a Na+ ion channel activated by hyperpolarisation (unlike normal vgc’s which are activated by depolarisation)
what are the three phases in the generation of pacemaker potentials
phase 4
phase 0
phase 3
what occurs in phase 4
RMP
If channels are activated
what occurs in phase 0
threshold value is exceeded
voltage gated calcium channels open
influx of calcium ions
depolarisation
what occurs in phase 3
voltage gated potassium channels open
efflux of potassium channels
repolarisation
what are the low resistance pathways between myocytes called that facilitate the conduction of electricity
intercalated discs - allows everything to contract at the same time because its very quick
why does the AVN slow down the rate of conduction
to allow ventricles to fill adequately
where does the AVN conduct this electricity
bundle of His and then to the purkinje fibres which allows both ventricles to be contracted together
what do atrial/ventricular cells have
a stable resting membrane potential
what are the five phases of AV node APs
phase 4 phase 0 phase 1 phase 2 phase 3
what occurs in phase 4
resting potential (around -90mv)
what occurs in phase 0
upon stimulation by electrical activity from the SAN the voltage gated sodium channels open allowing an influx of sodium into the cells causing depolarisation once threshold value is exceeded
what occurs in phase 1
repolarising phase and is the peak of the AP
what occurs in phase 2
plateau phase (lasts for about 200-400ms)
caused by opening of voltage gated calcium channels
causes calcium to influx in
but this is much slower and the channels stay open for longer
this causes a sustained depolarisation
what is the importance of the plateau phase
the myocytes are unexcitable (refractive) which means no twitching as only one AP produces a contraction. this is essential for proper ejection from the heart.
what is ventricular fibrillation
when there are loads of APs firing so the ventricles don’t get a chance to fill properly so theres no CO and on perfusion and death occurs
what occurs in phase 3
vgcc’s will close
vgkc’s will open
allows k+ to efflux
repolarisation occurs
what is contraction caused by
an increase in cytosolic Calcium levels during the plateau phase (calcium rises from 0.1 micro moles to 2 micro moles)
what two things that the rise in calcium cause
1) bind directly with troponin
2) bind to ryanodine receptors
how does calcium binding to troponin cause contraction
causes a conformational change and displaces tropomyosin allowing contraction
how does calcium binding with ryanodine receptors cause contractions
calcium binds to RyR receptors
RyR is an LGIC on the SR
this causes calcium induced calcium release
these calcium then also bind to troponin…
how does calcium induced calcium release occur in smooth muscles
IP3R
what does stimulation of sympathetic nerves in the heart have an effect on
heart rate
force of contraction
what heart rate also known as
chronotropic effect
what is the force of contraction also known as
inotropic effect
what sympathetic nerves innervate the SAN and ventricles
T1-T5
What do sympathetic nerves release and what receptors do they act on
NA which acts on beta 1 adrenoceptors
what does activation of the beta 1 adrenoceptors causes
an increase in pacemaker frequency causing an increase in heart rate (tachycardia)
what else does activation of these receptors cause
causes calcium channels to be open for longer
(beta 1 adrenoceptors are Gs coupled and so positively coupled with adenylate cyclase, so cAMP is increased and more PKA is activated which phosphorylates calcium channels and also phosphorylates potassium channels leading to hyperpolarisation. this leads it to hyper polarise quicker so that contraction is briefer which causes a greater influx of calcium) = increases force of contraction
what does stimulation of parasympathetic nerves have an effect on
heart contraction = chronotropic effect only
what parasympathetic nerves innervates the heart
vagus nerve from the brain innervates the SAN
what does the vagus nerve release
Act which acts on M2 receptors
what does stimulation of the M2 receptors do
M2 receptors are Gi and so are negatively coupled with adenylate cyclase and so cause a decrease in cAMP and theres less activated PKA and therefore calcium channels will be less open.
this causes a decrease in pacemaker frequency resulting in a decrease in heart rate (bradycardia)
