M7 L3 : Cardiac muscle Flashcards
Describe the structural organisation of the heart and atrial cells
Heart has 2 atria and 2 ventricles. Atrial cells have central nucleus with no t-tubules and contract quite weakly. They have gap junctions to allow electric activity to spread.
Describe ventrical cardiac cells
Ventricular cells are larger and are branched intercalated discs that prevent cells from separating during contraction. Contains gap junctions that allow coordinated contraction: APs carried from one cell to the next.
They have lots of mitchondria. 1-3 nuclei. t-tubules at the z discs and SR less developed
Where are action potentials initiated in the heart? Are they controlled by nerves
AP initated in cells in the right atria (sino atrial node). Cardiac muscle is myogenic: initates contraction without nervous input
Describe the stages of Ventricular myocyte AP
The action potential is long lasting >100 ms. depolarisation is due to Na+ channels opening and then it turns off.
- Plateau phase where there is a large sustained calcium current through voltage gated slow channels. Ca2+ binds to RyRa triggers the release of calcium into cytosol from the SR known as calcium induced calcium release.
- repolarisation when Ca2+ channels close and K+ channels activate bringing it back to RMP
How is the the membrane potential depolarised throughout most of the heart beat - tentani highly unlikely
Ca2+ entering from inside which triggers SR to release Ca2+ into cell as well balanced by Ca/Na+ exchanger which also brings in 3Na+ for every 1 Ca2+ so it makes the membrane more positive anyway
How is heart beating regulated
Since membrane is highly depolarised through most of the twitch it makes the refractory period longer so the refractory period is for most of the twitch. it cannot be re excited and summation of responses is impossible.
Heart beats 1 per second. What is the division of contraction and relaxation during that time
It contracts for 1/3 (peak of depolarisation) and relaxes for 2/3 (fills with blood)
compared to skeletal muscle what is the ratio of contracting and APs
skeletal: full Ap back down to RMP then full contraction
cardiac: AP long slow, contraction pretty near finished before AP starts repolarising
If you have a premature contraction triggered in the relative refractory period
its small and it won’t pump out the blood.
On a T tubule what provides the structural basis for ECCoupling
LTCC: I type voltage gated calcium channel (Ical) on T-tubule and then on the SR going around it are RyR= ryanodine receptors that are Ca2+ triggered calcium channels in the SR
What are the 4 main ways to get relaxation to occur
Ca2+ must decline allowing Ca2+ to dissociate from troponin. This requires active transport of Ca2+ out of cytosol by SR Ca2+ ATpase, Sarcolemma Na+/Ca2+ exchanger, Sarcolemma Ca2+ ATPase and mitochondrial CA2+ uniport
What are the main differences in trigger for Ca2+ release, contraction type for skeletal vs cardiac
Cardiac is electrically coupled, with Ca2+ release triggered by Ca2+ influx. It has graded contraction as troponin usually not saturated but has all fibres or none whereas skeletal is electrically isolated, Ca2+ release triggered by Na+ and all or none contraction as troponin is always saturated with ability to recruit more for graded
How is Cardiac output ( L blood that comes out of the heart per minute)
CO= Stroke Volume * Heart Rate
What sets the heart rate
The heart rate is set by pacemaker cells in the sinoatrial node. The rate can then be modified, especially via autonomic nerves releasing neurotransmitters
In pacemaker cells what are is different about their RMP
It is unstable, it has a slow spontaneous depolarisation due to leaky “If” channels letting Na+ in.
Your intrinsic heart rate is slightly faster than your resting rate. Why
At rest your parasympathetic nerve (vagus nerve) activity is high- releasing ACh which hyperpolarises RMP and slows the rate of discharge of SA cells and reduces heart rate.
What does sympathetic nerves do
releases Noradrenaline which has 4 effects on the heart via cAMP and protein kinase A.
Noradrenaline increases the rate of spontaneous depolarisation. Also increases amplitude of ICa and increases uptake of Ca2+ to be released-> more Ca2+ in cell
What is stroke volume and how is it increased
reflects the tension developed by cardiac muscle fibres in one contraction. Can be increased by :
Increasing rate of firing (heart rate or HR), increased stretch of ventricles (length) and certain neurotransmitters
Describe the modulation of force by altering stimulation frequency (automaticity)
Increasing heart rate increases contractile force (SV) this is because there is less time available between APs for Ca2+ to be pumped out the cell. There is a higher average Ca2+ level and this exposes more troponin binding sites.
What is the modulation of force by muscle length : active and passive tension
The active tension component in cardiac muscle is the same as skeletal as it has same structure for myofilaments. However Heart has collagen in it and organisation of cardiac connective tissue so passive tension only increases as it is stretched. What this means is that the more you stretch a heart (ie put blood in it) the harder it will contract against it.
What is starlings law of the heart? intrinsic or extrinsic
as the resting ventricular volume is increased the force of contraction is increased up until a threshold. Intrinsic
What is the neural control of stroke volume : sympathetic nerves
Noradrenaline acts on Beta receptors (g protein) and via second messengers. Bigger contraction = more calcium. It acts on L-type channels resulting in more calcium entering the cell and Ca2+ pump in SR so it increases Ca2+ stores.
Net result is bigger/shorter contraction. It also upregulates Ca ATPase to get Ca back into SR so AP shortens because you’re removing Ca2+ quicker
Increased sympathetic stimulation results in
increased output at any filling pressure due to increase in inotropy (contractility) and heart rate
How does the AP started in the sinoatrial node spread throughout the atria to the ventricles (which cell)
through Purkinje cells
How can the calcium influx in the first stage of Excitation contraction coupling be balanced and what stimulates it
Na+/Ca2+ exchanger in the sarcolemma which is stimulated by the repolarisation phase.
