Lecture 2 - EC coupling Flashcards
Going through lecture material
function of intercalated discs
allow impulses to travel rapidly between adjacent cells so they function as one rather than individual cells
what is E-C coupling
converting an electrical stimulus into a mechanical response
action potential –> contraction
Define ‘ action potential’
a short-lasting event in which the electrical membrane potential of a cell rapidly rises and falls following a consistent trajectory
list some features of action potentials
- resting and threshold potential
- occurs in excitable cells ( neurons / muscle cells )
- generated by special voltage-gated ion channels
- depolarisation / hyperpolarization
AP stage 1
resting potential -90mV transient potentials move the depolarisation threshold (-67mv)
AP stage 2`
- 67mV threshold reached and action potential initiates
- rapid voltage change due to influx of Na+ ions
AP stage 3
+50mV efflux of K+ ions
AP stage 4
hyperpolarization due to excess K+channels remaining open
depolarisation is not possible during this stage
Sodium concentrations
Extracellular 135-145mmol/L
Intracellular 10
Potassium concentrations
EC 3.5-5.0
IC 155
Chloride
EC 95-110
IC 10-20
Absolute refractory period
impossible to evoke another action potential
Relative refractory period
a stronger than usual stimulus required
Ventricular AP phase 0
resting potential -85-95
depolarizing impulse activates fast Na+ channels and inactivates K+ channels
V AP Phase 1
early repolarization phase
transient opening of K+ and closing of Na+
V AP phase 2
plateau phase
Ca2+ channels open
key difference between nerve AP
V AP Phase 3
Repolarization phase
Ca2+ channels inactivate
K+ channels open
V AP refractory period
Na+ channels are inactive until membrane is repolarised
SA node pacemaker potential phase 0
Rapid depolarisation
due to L-type Ca2+ channels opening
SA node pacemaker potential phase 1-3
rapid hyperpolarisation due to K+ channels
SA node pacemaker potential phase 4
unstable resting potential
due to funny/fast Na+ channels
MP-reaches threshold potential
define automaticity
a pacemaker cell’s ability to spontaneously depolarise reach threshold and propagate an AP
How are action potentials conducted to myocytes
via gap junctions
role of calcium in EC coupling
depolarization of muscle cell surface to release of Ca2+ in SR
controls Ca2+ within muscle and Ca2+ controls force of contraction
Role of calcium in muscle contraction
- in the plateau phase Ca2+ enters–> there is small increase in intracellular Ca2+
- Ryanodine receptors ( SR surface )detect this positive feedback induced releasing more Ca2+ –> produces calcium sparks
- spatial + temporal summation of 30,000 sparks leads to a cell-wide increase in cytoplasmic Ca2+ concentration
Whats in muscle contraction?
- Calcium binds to troponin C, moving the tropomysin complex off the actin binding site allowing the myosin head to bind to the actin filament
- The myosin head uses ATP hydrolysis to pull the actin filament towards the center of the sarcomere
- Intracellular Ca2+is taken up by SR ATPase pump back
- intracellular calcium concentration drops and troponin complex returns over the active site of the actin filament which ends contraction
Length of refractory period in cardiac muscle
Long, therefore the cardiac muscle cannot sum action potentials or undergo tetanus
How long does the effective refractory period last for?
duration of the AP
prevents tetanic contraction so the muscle relax allowing venous blood to refill the heart
Purpose of a shorter EPI AP?
ensures ENDO is still refractory during EPI repolarisation and cannot be activated by EPI
Features of ENDO refractory period
longer than time taken for the AP to propagate from ENDO to EPI plus the EPI AP duration
What happens if EPI repolarization occurs outside the ENDO refractory period
depolarised EPI tissue may reactivate the ENDO causing a re-entry cyclic arrhythmia to be set up
