Muscle [Cardiac] Flashcards
Structure of atrial cells
No t tubules. Contract weakly. Gap junctions.
Structure of ventricular cells
Larger, branched, gap junctions, t tubules.
Pathway of action potentials in the cell
Initiated in the right atria in the sino-atrial node. Spreads through the atria via conducting cells (purkinje) to the ventricles.
How is Ca2+ able to stay in the cell to keep AP longer?
lCa produces Ca influx into cell through slow channels. This triggers SR channels to open. The increased calcium is balanced by the Na/Ca exchanger. Cell is kept depolarised bc not many K+ channels are open
What does the Na/Ca exchanger pump in and out and what is the effect of this?
Pumps in 3Na+
Pumps out 1 Ca2+
What is the AP like if triggered during the refractory period?
Smaller as wouldn’t get much blood therefore tension.
Timing of AP and contraction skeletal vs cardiac
Skeletal: AP during absolute refractory period then nothing during relative.
Cardiac: AP and contraction finish at the same time and start at the same but. But are just different shapes.
LTCC
L-type voltage gated ca2+ channel (lCa) in t-tubule.
Can initiate contraction with this.
What is the difference between skeletal and cardiac muscle in terms of troponin?
Cardiac: troponin has only one calcium specific site.
Skeletal: has two
Is the troponin in cardiac muscle more or less saturated than skeletal and why?
Not fully saturated with calcium due to the calcium transient (curve?) being a lower amplitude.
What type of pump is the Na/Ca exchanger? Like how is it stimulated?
Voltage-gated. Stimulated by repolarisation phase.
2 ways to get rid of Ca2+
SR ATPase
Sarcolemma Na/Ca exchanger
What are pacemaker cells? where are they found?
They are found in SA node of right atria. Reflects tension developed during contraction.
Parasympathetic nerve
Vagous nerve. decrease heart rate by releasing ACh. Slows rate of discharge of SA cells. takes longer to reach threshold.
Sympathetic nerve
Increase HR by releasing NA which increases the rate of depolarisation.
Pacemaker potential
Leaky to Na+ so depolarises in a diagonal line up before the curve starts. Therefore unstable RMP.
3 ways to increase SV
Can increase by increasing rate of firing, stretch or neurotransmitters.
Modulation of force by altering stimulation frequency
More calcium stays, more calcium in SR, more calcium released from SR, new steady state.
Modulation of force by muscle length overview
More stretch, more fill, more contraction and active force. More passive force.
More Ca2+, more contraction force.
When does cardiac muscle have max active force? And when does passive force start rising rapidly? What’s the stretch limit?
2.1 max active force.
2.0 afterwards passive
Can’t go beyond 2.4
Starlings law
Resting ventricular volume is increased, force of contraction of ventricle is increased.
How does NA affect SA node cells and therefore increase force?
Increases f of discharge of SA node cells which increases f of AP therefore contraction.
How does NA increase force of contraction through ICa?
Increases amplitude of ICa which means more Ca enters cell each beat. Have less time for Ca to exit too.
How does NA increase force of contraction through SR calcium pump?
Takes up more calcium, SR releases more Ca.
How does NA increase force of contraction through action and myosin?
Decreases their sensitivity for calcium. But this is masked by an increase in the amount of Ca. However it means the cell can relax more quickly so more time to fill.
What is the net effect of modulation of force by neurotransmitter NA?
Bigger but shorter AP.
What 2 things does NA act through?
cAMP and kinase A
