Session 4- Electrical and Molecular Mechanisms in the Heart and Vasculature Flashcards
what is the resting membrane potential of cardiac myocytes
-85mv
what triggers action potentials in myocytes
increase in cytosolic (Ca2+)
how long does the action potential last in a cardiac ventricle
sino atrial node
100ms
100ms
cardiac action potential
- opening of V-gated Na+ channels
- transient outward K+ current
- opening of V-gated Ca2+ channels (some K+ channels also open)
Ca2+ channels inactivate and voltage gated K+ channels open
what is threshold of cardiac action potential
+30mv
sino atrial node action potential
- pacemaker potential influx of sodium ions
- slow depolarisation
- opening of V-gated Ca2+ channels
- opening of V-gated K+ channels
features of the pacemaker potential
activated at membrane potentials that are more negative than -50mv
initial slope to threshold- I f funny current
the more negative, the more it activates
what causes the upstroke/downstroke in the SA node action potential
opening of voltage gated Ca2+ channels
down stroke- opening of voltage gates K+ channels
why are cardiac myocytes so sensitive to changes in potassium ions
k+ permeability dominates the resting membrane potential
what is hyperkalaemia
plasma K+ concentration is too high >5.5mmolm.L ^-1
what is hypokalaemia
plasma K+ concentration is too low >3.5 mmol.L^-1
effects of hyperkalaemia
Ek gets less negative so the membrane potential depolarises a bit
this inactivates some of the voltage gates Na+ channels
- slows upstroke
- shorter AP - more rapid repolarisation
hyperkalaemia depolarises the myocytes and slows down the upstroke of the action potential
risks with hyperkalaemia
the heart can stop- asystole
may initially get an increase in excitability
depends on extent and how quickly it develops
how do you treat hyperkalaemia
calcium gluconate- reduce excitability
insulin and glucose- promotes movement of sodium ions in cell
these wont work if heart has already stopped
effects of hypokalaemia
lengthens action potential
delays repolarisation
problems of hypokalaemia
longer action potential can lead to early after depolarisation
this can lead to oscillations in membrane potential
can result in ventricular fibrillation
mechanism due to the way the K+ channels behave
how does cardiac muscle contraction occur
- depolarisation open L-type Ca2+ channels in T-tubule system
- localised Ca2+ entry opens Calcium-induced calcium release channels in SR
- close link between L-type channels and Ca2+ release channels
- 25% enters across sarcolemma, 75% released from SR
relaxation of cardiac myocytes
must return [ca2+] to resting levels
most is pumped back into SR
-raised Ca2+ stimulates the pumps
some exits across cell membrane
- sarcolemmal Ca2+ ATPase
- Na+/Ca2+ exchanger
excitation contraction coupling at the vascular level
depolarisation opens VGCCs
4 calcium ions bind to calmoldulin
MLCK binds to calmodulin
MLCK + calmodulin phosphorylates myosin head
at the same time noradrenaline activates alpha 1 receptors stimulating calcium release
G alpha q causes the formation of DAG and IP3
DAG activates protein kinase C which inhibits MLCP
MLCP dephosphorylates myosin head which would inactivate it PKC prevents this
IP3 causes the release of calcium from the sarcoplasmic reticulim
what enables the actin-myosin interaction
myosin light chain must be phosphorylated
