CFB L4 Flashcards
What is a myogenic contraction?
Heart consists of heart muscle cells - myocardial cells
Myocardial cells are contractile
1% of mycocardial cells are specialised to produce action potentials simultaneusly
Therefore, waves of excitations apread through the heart causing myocardial cells to contract in a coherent way
The heat has a myogenic contraction - the heart contracts independent from outside signals from nervous system etc
Signal is from autoryhtmic cells - in the pacemaker, therefore, signal to start contraction is in pacemaker
State structural differences between cardiomycotyes and autoryhthmic cells
- Autorythmic cells are smaller, cardiomyocytes are larger
- In autorythmic cells, not organised into sarcomeres, whereas in cardiomyocytes, contractile fibres organised into sarcomeres
- Autoryhmic cells do not contribute to contraction force, cardiomyocytes are striated muscle and do contribute largely towards contraction force
State structural differnces between cardiomyocyytes and skeletal muscle
Cardiomyocytes Large mitochondria,
single nucleus
State structural simaliries between cardiomyocytes and smooth muscle
single nucleus
Electrically connected via gap junctions
Work as a functional syncytium
State which stucture present between cardiomyocytes contains gap junctions
Intercalated disks
State the function of intercalated disks
Point where neighbouring cardiomyocytes branch and join
They are cross bands of thickening sarcomere
Contain
-Desmosomes molecular complexes of adhesion proteins- allow tight junctions to form between cardiomyocytes
-Gap junctions - MEMBRANE PROTEIN CHANNELS electrical connections between cardiomyocytes, transfer of electrical impulses and ions
Therefore, this allows depolarsiation to spread rapidly across cardiomyocytes allowing them to work as a functional syncytium
Describe the generation of action potential in myocardial contractile cells
Resting membrane potential (phase 0) -
stable resting membrane potential of -90mV
Depolarisation phase (phase 4):
- Starts with a wave of depolarisation entering cells from gap junctions (spontaneously initiated by autorythmic cells)
-Membrane potential becomes more +ve
-Na+ channels open
-Na+ enters
-Depolarisation of cell
-Activates voltage gated Ca2+ channels
-Ca2+ channels slowly open
-Some Ca2+ enters
-Membrane potential reaches =20mV
-Na+ channels close, no more entry of Na+
Initial repolarisation phase - phase 1
-As Na+ channels close, K+ channels open
-K+ leaves briefly
-Ca2+ channels still opening
-Ca2+ still entering cells
Plateu phase 2:
- Ca2+ channels finally fully open
-Ca2+ infux
-This causes K+ channels to temporarily close
-More Ca2+ influx than K+ efflux, increased Ca2+ influx, decreased K+ eflux, leads to platau of action potential, prolongued action potential
prolongued action potential prevents
-sustained muscle contraction
-prevents premature muscle relaxation
-prevents ventricular filling when muscle is contracting
Rapid Repolarisation Phase 3
- Ca2+ channels close
-No Ca2+ influx
-K+ channels reopen
-K+ efflux
-Rapid repolarisation to stable resting membrane potential - 90mV
How do autorythmic cells generate action potentials simultaneously without the help of the nervous system?
- Exhibit UNSTABLE membrane potential of -60mV
-This slowly depolarises up to the threshold, which causes action potential to fire
-This -60mV is known as pacemakrer potential - not resting potential
What allows autorythmic cells to exhibit an unstable membrane potential of -60mv ?
Funny current channels (If)
Permeable to both, Na+ and K+ ions
Part of a family of HCN channels
Describe the events leading to an action potential in autoryhtmic cells
Pacemaker potential / unstable potential: -60mV
Leads to opening If channels
When negative membrane potential, more Na+ influx than K+ efflux
Therefore, SLIGHT depolarisation as membrane SLOWLY becomes more +ve
If channels slowly close
Slight depolarisation by Na+ influx
Causes Ca2+ channels (T type) to open
Influx of Ca2+, depolarises cell + moves the membrane towards threshold
As membrane potential reaches threshold, second set of Ca2+ channels open (L type), rapid influx of Ca2+, steep depolarisation, action potential
Rapid repolarisation: Ca2+ channels close, slow K+ channels open, K+ efflux, membrane potential: -60mV
`Why do autoryhmic cells not have a resting state?
As they are repolarised and the membrane potential reaches -60mV, funny current (IF) channels open again, and the process of depolarisaion starts again
Due to IF channels
Permeable to both, Na+ and K+
How does an action potential generated by the autorthmic cells bring about muscle contraction?
Action potential generated by autoryhmic cells reach contractile cells via gap junctions
Initiates ECC - Excitation Contraction Coupling
Define ECC
Excitation Contraction Coupling: where electrical stimulus (action potentials) converted into mechanical response (muscle contractions) in contractile cells
Describe the processes which occur during ECC
- Action potential travels through sarcolemma, to T tubules
- Causes Ca2+ channels (L type) to open in T tubules
- Ca2+ released into cell
- Causes Ryanodine Receptor Ca2+ release channels in sarcoplasmic reticulum to open
- Ca2+ leaks out of sarcoplasmic reticulum into cytosol
This process is called Ca2+ induced Ca2+ release CICR - 90% of Ca2+ needed for contraction released by CICR, rest come from extracellular fluid
- Ca2+ in cytosol binds to contractile elements, troponin - cross bridge formation sequence + sliding filament movement, leading to contraction
- As Ca2+ decreases in cytosol, unbinds from troponin, myosin releases actin, contractile filaments slide back to original position
State why EC coupling is dependent on CICR
CICR - Ca2+ induced, Ca2+ release
Ca2+ must bind to ryanodine receptor Ca2+ release channels to open them, allowing Ca2+ to be released into the cytosol
