How does the cross-bridge cycle differ between smooth, skeletal, and cardiac muscle?
it doesn't. It is exactly the same for all of them.
length and diameter of cardiac muscle cells
ventricular: 100μm x 30μm atrial: 100μm x 10μm
define myogenic and sate its relevance to cardiac muscle cells
myogenic means that control over muscle cells is involuntary. This is the case with cardiac muscle cells.
T-tubules in cardiac muscle (vs. skeletal)
in cardiac muscle they are in the ventricles at the Z-lines, thus, there is only 1 T-tubule per sarcomere (as opposed to 2 in skeletal). N.B. atrial muscle cells have no T-tubules.
is there a sarcoplasmic reticulum in the cardiac muscle or nah?
sarcoplasmic reticulum is present, however, it is not as extensive or as important as in the skeletal muscle.
intercalated discs (contain? functions?)
- desmosomes prevent cells from separating during contraction - gap junctions allow APs to carry between cells - allows for the coordinated contraction of all myocytes
action potential in the ventricular myocytes
- long lasting (greater than 100ms vs. 1ms in skeletal) - plateau (due to Ca2+) - very little chance of tetani
found at the top of the right atrial wall. Initiates the AP.
carry AP, from the atroventricular node, around the ventricles .
rapid depolarisation (ventricular myocytes) due to...
fast voltage-gated Na+ channels, cause the membrane potential to reverse from -90mV to +30mV
Plateau phase (ventricular myocytes) due to...
long acting, voltage-gated L-type Ca2+ channels open and there is a large sustained Ca2+ current, as the calcium moves in from the extracellular fluid
repolarisation (ventricular myocyte) due to...
closing of Ca+ channel and opening of K+ channels (basic AP tekkers)
how does the interaction between the SR and the T-tubules differ in cardiac vs. skeletal?
in cardiac muscle there is a separation between the SR and the T-tubules
how is the influx of Ca2+ into the myocytes balanced?
Dihydrogen pyridine - same exact thing as L-type Ca2+ channel
influx of Ca2+ into the sarcolemma/T-tubules, triggers?
CALCIUM INDUCED CALCIUM RELEASE Ca2+ sensitive channels in the SR (RyRa) open, liberating BURSTS (not constant) of Ca2+. Muscle contraction can then occur as it does in the skeletal muscle.
as the action potential starts to repolarise, what happens to the Ca2+ ions?
Pumped into the SR through CaATPase (SERCA) and extruded from the cell via Na/Ca exchanger
how is the contraction size graded?
by changing the concentration of Ca2+ i.e the presence of actin binding-sites
can the heart increase the force in a contraction by recruiting more fibres?
NO!!! "all or nothing" when the heart beats, every muscle fibre is involved
Cardiac output (CO) =
Stroke volume (SV) x Heart rate (HR)
Stroke volume reflects...
tension developed by the cardiac muscle fibres in one contraction
3 ways to increase stroke volume
1. increased stretch of ventricles (length) 2. increased rate of firing (HR) 3. certain hormones
the pacemaker cells are...
Sinoatrial node and atrioventrical node
unstable resting membrane potential, spontaneously reaches threshold
threshold is reached (spontaneously) when there is a slow depolarisation, due to 'funny' channels letting Na+ leak into the cells
when the threshold is reached, the Ca2+ T-type (transient) channels open and the rapid influx of Ca2+ produces the rising plane of the action potential
inactivation of Ca2+ channels and opening of K+ channels. Takes a while due to the L-type Ca2+ channels
3 ways to increase HR (by altering the SA depolarisation)
1. decreasing the threshold potential 2. make the maximum distolic potential more positive 3. increasing the rate of spontaneous depolarisation
parasympathetic vagus nerve
- decreases heart rate - releases ACh - mostly affects the HR
sympathetic cardiac nerve
- increases heart rate - releases noradrenaline - affects both HR and SV