Excitable tissue, muscle lecture: 3 Flashcards
Describe the intercalated discs of cardiac myocytes:
Intercalated discs: • Desmosomes prevent cells from separating during contraction • Contain gap junctions that allow the action potentials to be carried from one cell to the next • Allows for the co-ordinated contraction of all the myocytes (unlike skeletal muscle where fibres are recruited via the motor nerves)
All the mycocytes of he heart are connected, whats the word to describe this:
Syncytium
Describe the action potential of the cardiac myocyte: (insert pic)
3 major stages (0,2,3)
0 – Rapid depolarisation due to fast voltage- gated Na+ channel
2 – Plateau phase due to slow voltage gated Ca2+ channel (L-type Ca2+ channel)
3 – Repolaristation due to closing of Ca2+ channels and opening of K+ (outward) channels
How does the cardiac AP differ to skeletal?
- Action potential is long lasting > 100 ms long
- Has plateau phase due to presence of a large sustained Ca2+ current (ICaL) (SLOW L TYPE CA CHANNELS)
- Membrane potential depolarised throughout most of the “twitch” (heart beat)
- Summation/tetani of cardiac muscle highly unlikely
Whats the absolute refractory period and relative refractory period of cardiac mycoytes?
ARP: ~200ms
RRP:~250ms
Describe the major flow of ions during each stage of the cardiac AP:
insert pic
What is the structural basis for Excitation contraction coupling in cardiac myocytes:
T tubules contain:
- NCX (removes Na and allows Ca in (to balance and prevent excessive deloparisaiton)
- L type voltage gated Ca channels
- Na/K ATPase
Basically T tubules depolarise with the Sarcolemma, This opens the L type Ca channels (DHPR), Ca flows and binds RyR on the sarcolemma, and this induces Ca release. (the DHPR and RyR are aligned)
Na/K ATPase create the electrical gradient.
Describe cardiac muscle excitation contraction coupling:
- Depolarization opens voltage-gated fast Na+ channels in the sarcolemma. Reversal of membrane potential from –90 mV to +30 mV
- Depolarization wave opens slow (L-type) Ca2+ channels in the sarcolemma (DHPR)
- Ca2+ influx balanced by a Na+/Ca2+ exchanger
• Ca2+ influx triggers opening of Ca2+-sensitive channels in the SR (RyRa), which liberates bursts of Ca2+ (i.e. calcium induced calcium release)
RyRa
• The raised intracellular Ca2+ concentration allows
Ca2+ to bind to troponin, which then switches on the contractile machinery (cross bridge cycle)
Describe how relaxation occurs in the cardiac mycote:
For relaxation to occur [Ca2+]i must decline, allowing Ca2+ to dissociate from troponin.
This requires Ca2+ transport out of the cytosol by four pathways (in green):
• SR Ca2+-ATPase (SERCA) (majority is this)
• sarcolemmal Na+/Ca2+ exchange (NCX)
• sarcolemmal Ca2+-ATPase (NOT SERCA)
• mitochondrial Ca2+ uniport.
What is cardiac output?
Volume of blood pumped out of the heart per a minute
CO = HR x SV
HR = Heart rate SV = stroke volume, the volume of blood in the ventricle.
What determines heart rate
Heart Rate (HR) is set by the pacemaker cells in the sinoatrial node. The rate can then be modified, especially via the autonomic nerves releasing neurotransmitters.
What influences stroke volume?
Stroke volume (SV) reflects the tension developed by the cardiac muscle fibres in one contraction. Can be increased by:
• increased rate of firing (heart rate/HR)
• increased stretch of ventricles (length)
• certain neurotransmitters (e.g. Noradrenaline)
What are the pacemaker cells of the heart?
Sinoatrial node
AV node (dont need to understand yet, next sem)
Describe the action potential of the pacemaker cels:
- Pacemaker potential: Slow depolarisation is due to funny current (Na drive) (unstable resting membrane potential) (this is not the rapid Na influx usually seen after threshold is reached)
- Depolarization: At threshold, Ca2+ channels open. Explosive Ca2+ influx produces the rising phase of the action potential, sustained by opening of slow Ca2+ channels. (different from normal as Na usually drives this part)
- Repolarization is due to Ca2+ channels inactivating and K+ channels opening.
Describe the autonomic innervation of the heart:
Autonomic = Autonomic nervous system i.e regulates body without need for any conscious input
Heart:
- Parasympathetic = vagus nerve, releases Ach, slows heart rate
- Sympathetic = cardiac nerves, release noradrenalin increase HR and contractile strength
Describe the neural control of the heart again:
Via alteration of pacemaker potential
Vagal nerves release acetylcholine (ACh): Decrease rate of spontaneous depolarization and hyperpolarises the resting membrane potential = decrease heart rate
Sympathetic nerves release noradrenaline (NA): Increases rate of spontaneous depolarization = increase heart rate
What is “automacity” in reference to the heart?
• Increasing heart rate increases contractile force (stroke volume)
- due to less time available for Ca2+ to be pumped out of cell
What does the length tension relationship look like in muscle?
(just be able to recognise)
insert pic
What is notable about the length tension relationship in muscle?
- Increased stretch (ventricular filling=preload) results in more force developed (stroke volume)
- Starlings law of the heart: “as the resting ventricular volume is increased the force of the contraction is increased”
- entirely intrinsic!
i.e when you exercise more blood returns to the heart, it fills to a higher degree and consequently contracts harder, ejecting more blood.
Describe the neural influence on stroke volume:
Noradrenaline (NE = NA) acting on β receptors and via second messengers acts on:
• L-Type channels resulting in more calcium entering the cell.
• Ca2+ pump in SR so SR increases its Ca2+ stores
Net result = bigger/shorter contraction
Describe again the neural influence on stroke volume but now with reference to action potential phase.
Noradrenaline released by sympathetic nerves leads to increased cytosol calcium due to increased HR shortening time for extrusion
And via second messengers (previous slide) :
- by increasing Ca++ influx (via Ca++ channels) during the action potential (primarily during phase 2),
- by increasing the release of Ca++ by the sacroplasmic reticulum (due to greater SR uptake)
Increased sympathetic stimulation results in increased output at any filling pressure due to increase in inotropy and heart rate
Compare and contrast the conductivity of skeletal and cardiac muscle:
Skeletal : Electrically isolated
Cardiac: electrically coupled (intercalated discs, syncitum)
Compare and contrast the trigger for Ca release from the SR in skeletal and cardiac muscle:
Skeletal = Na
Cardiac = Ca
Compare and contrast how Ca and recruitment of more fibres influences contraction in skeletal and cardiac muscle:
Skeletal: (Ca) Contraction is always all or none (troponin always saturated). Recruitment of more fibres (yes) contraction always graded
Cardiac: (Ca) Contraction graded, troponin not saturated. (cant recruit more fibres as all fibres or none)
