Physiology: cardiac muscle function Flashcards
Cardiac muscle cells size?
100um x 15 um
Cardiac muscle cell has slow or fast diffusion of oxygen?
Fast diffusion of oxygen
Cardiac muscle cell structure?
Striated (2um repeat)
Cardiac muscle cell contains?
Numerous mitochondria (30% cross-sectional area) -> energy from oxidative phosphorylation
Cardiac muscle cells are electrically coupled end-to-ed by ______.
Connexin 43
Transmembrane proteins creating a barrel structure for what?
Ion movement for the transmission of electrical current
End part of each cardiac muscle fibre has _______ with the next fibre to increase surface area to hold cells together and to allow ________.
interlaced fingers; electrical current movement
Ventricular cells are not __________ (steep rise in membrane potential) unlike pacemaker cells and remain _____ for a while.
spontaneously active; depolarised
Cardiac muscle action potential triggers _____ whose time to peak is comparable to the action potential duration.
Contraction
Force of action potential starts to drop off with ______.
Repolarisation
Action potential of cardiac muscle cell has ______ (300 millisecond duration (2 ms AP peak for skeletal muscle).
Long plateau
Describe the sodium channel
- Fast
- Inward
- Causes depolarisation of action potential
- Sodium stimulates calcium channel
- Similar to nerve and skeletal muscle
- Crucial for fast AP propagation across the myocardium.
Describe the calcium channel
- Slow channel
- Inwards
- Maintains long plateau of AP
- Entry of calcium contributes to excitation-contraction coupling
- Target of calcium channel blocking drugs (reduce contractility)
Describe the potassium channel
- Efflux of potassium is repolarising
- voltage sensitive and sensitive to intracellular constituents e.g. ATP and calcium
Arrhythmias are often triggered by?
Triggered by ischaemic events causing ectopic foci and/or re-entry circuits i.e. out of sequence contraction that can trigger abnormal rhythms.
- Other causes: hormonal adrenaline or mutations in channels (e.g. long QT syndromes)
What are T-tubules and what do they contain
They are a continuation of surface membrane and contain voltage-gated calcium channels located particularly at the dyads.
Where are T-tubules located?
Dyads. Where sarcoplasmic reticulum (SR) meets the T-tubule is the dyad.
Calcium is pumped into SR.
Describe steps of contraction
- calcium pumped into SR
- Once T-tubule comes down with AP, T-tubule calcium channels open
- Calcium enters into cytoplasm in interstitial fluid
- Triggers activation of release channels in the dyads
- Causes release of even more calcium from SR
- Calcium binds to troponin and contract cardiac muscle
Describe the steps of excitation-contraction coupling
- Action potential depolarizes T-tubule membranes
- Activates calcium channels in T-tubules resulting in a small calcium entry into ECF
- Calcium binds to calcium release channels in sarcoplasmic reticulum (SR): calcium-induced calcium release (CICR)
- Large calcium release from SR intracellular stores causes contraction.
- Relaxation occurs.
List steps of large calcium release from SR intracellular stores causing contraction
- Calcium released from intracellular stores
- Calcium in cytoplasm rises
- Calcium binds to troponin C
- Exposure of myosin-binding sites on the actin filaments.
- Cross-bridge cycling begins
- Active tension
- z-lines pulled together
Describe relaxation of muscle
- Slow inactivation of the calcium channel in the T-tubules
- Uptake of calcium ions into the SR by the SR calcium pump.
- Removal of calcium ions from the cell by the sodium/calcium exchanger (calcium back into T-tubule)
Factor of greater force of contraction?
Greater the intracellular calcium
Describe steps of adrenaline/noradrenaline in nerve synapse
- Binds adrenoceptor on ventricular cell surface which
- Activates G-protein to increase cAMP which
- Activates cAMP-dependent kinases which
- Phosphorylates effector proteins:
i) Voltage-gated calcium channel on the surface of T-tubules: increased inward calcium ions.
ii) Phospholamban (regulatory protein acting on the SR calcium pump to make it act faster: increases calcium uptake by SR calcium pump so that there is more storage for next contraction, allowing for stronger contraction. - Both actions increase peak SR calcium release and force but shortens time-course of systole.
Increasing peak sarcoplasmic calcium ion release and shortening systole leads to?
- Increase in amplitude of the AP.
- Stronger but briefer systole due to the phospholamban.
- Shorter diastole and time of contraction.
Cardiac glycosides act on?
Act on Sodium-potassium pump instead
Cardiac glycosides inhibit?
Inhibits the sodium pump -> sodium inside so sodium exchange is less effective, and less calcium is pumped out by the sodium/calcium exchanger.
Cardiac glycosides increases?
Increases intracellular sodium and increases cytoplasmic and SR calcium so progressively more calcium is available each cycle for contractile apparatus.
Effect of cardiac glycosides
Increases in peak calcium level so increased force of contraction but no decreasing in cardiac cycle.
Advantages of heart exclusively using aerobic method (due to high energy requirements)
- Very efficient in ATP production (38 ATP/glucose unit)
- Large blood supply (to provide sufficient oxygen
- Loaded with mitochondria
- Small diameter cells - facilitates adequate oxygen diffusion
- Not susceptible to fatigue - ATP production keeps pace with consumption.
Disadvantages of heart exclusively using aerobic method (high energy requirements)
- Entirely dependent on aerobic metabolism (unlike skeletal muscle)
- Critically dependent on blood supply
- Risk of heart attacks (damage caused by block of blood supply)
- Mitochondria density limits force production.
