21. Heart stuff not sure exactly Flashcards
2 types of cardiomyocytes
Working- involved in pumping function of heart
Conduction/pacemaker- form excitation/conduction system of heart.Pacemaker cells are smaller and lighter with rounded shape, that contain less
contractile elements and mitochondria.
Morphological features cardiac muscle
Striated: filaments arranged in sarcomeres
Smaller in size,
mononuclear
connected by intercolated disks (btw endings of each cell)
What is the function of the intercalated disks
They build up mechanical connections using desmosomes so cardiomyocytes are held tightly together
This is a necessary prerequisite for
performing the pumping function of
the heart.
Gap junctions in cardiomyocytes
Located in the peripheral part of the disks
Type of synapse so allows excitatory process from one cell to another
Do cardiomyocytes have a well developed T tubule system
YES
imp for making link btw excitation and contraction
condicts the AP from sarcolemma to sarcoplasmic reticulum
What are cisterns and diads
Myofibrils are enveloped by SR
The T-tubules and the terminal
branches of the SR called cisterns
together form a structures called
diads.
Many mitochondria found in them bc cardiomyocytes rely on aerobic metabolism
What is resting membrane potential of cardiomyocytes
-90mv
What are the 3 layers of the heart
Which layer is more suspectable to stretching
endocardium,myocardium, epicardium/pericardium
epicardium stretches so heart can take in greater amounts of blood - when heart is filled more, it contracts stronger
Are ventricular cardiomyocytes connected with atrial cardiomyocytes
NO
Connected via conducting system
Imp bc 2 functional synctiums ( atrial/ventricular)
Do pacemaker cells have a stable resting potential
no
Both cells generate action potentials
How do cardiomyocytes generate action potential
PHASE 0: Steep depolarization due to Na+ voltage gated channels open until +35 mv
PHASE 1: short term, small amplitude repolarization due to K+ channels opening and inactivation of Na+ channels
PHASE 2: Plateu. Membrane potential retained at 0Mv bc some K+ close and Ca2+ channels open which are also voltage gated but inactivated more slowly than Na+
PHASE 3: Opening of several types of K+ channels leads to repolarization
PHASE 4: resting memebrane potential
What is the biological significance of long duration of phase 2
To increase intracellular Ca2+ concentration
The entry of calcium ions into the cell causes calcium ions to be released by the SR for excitation/ contraction coupling
THIS IS CALCIUM DEPENDENT CALCIUM RELEASE
Their DHP recptor lets in more calcium ions than in skeletal
What is the result bc duration of contraction and action potential is same
No tetanus in the heart (when it doesnt hv time to fully relax)
When is absolute refractory period
Very long (toprevent tetanic contraction) bc there are no Na+ channels at phase 2.3.4
ARP starts at the beginning of phase 0 and
ends around the middle of phase 3 and MP
of -50 mV.
ARP coincides with the period of systole
and the onset of diastole.
During this period, myocardial cells cannot
be re-excited!
What is the supranormal period
Period hwere fast Na+ channels are responsive near threshold
weaker than normal stimulus will cause action potential
But these contractions are useless
What is automaticity of the heart
Ability of pacemaker cells to generate action potential without need of external stimuli
Due to spontaneous depolarization of their cell membranes
Conducted to working cells by gap junctions
Generation of action potential in pacemaker cells
Phase 4
It is generated by pacemaker channels
also called “If” channels, during phase
4 of the membrane potential (MP) in
pacemaker cells.
These channels open spontaneously as
the MP returns to its resting value of
-60 mV.
Leads to Na+ entry and K+ exit.
Na+ depolarize and at -50mv, T type Ca2+ channels open where threshold met t -40mv
Phase 0 and 3 of pacemaker AP generation
PHASE 0: Once threshold of -40mv met, L type Ca2+ channels open
PHASE 3: The repolarization phase is
associated with the opening of
several types of potassium channels
and the release of K+ from the cell.
MP returns to its resting value (-60
mV) leading to opening aging of
pacemaker channels.
SA node is pacemaker of our heart.
What has to happen to it to be our heart rate
Has to be suppressed
w/o innervation it contracts 105-110/min so has to be suppressed to get to 65-85/min
How is excitation conducted from atria to ventricles
- AP generated in right atrium, SAN
- Impulse conducted to AVN an dleft atrium
- AP delayed in AVN, allows atrai to fully contract
- AP to Bundle of HIS near interventricular septum
- AP spreads along Purkinje fibers which disperses it to rest of cells
Where is the highest and lowest sponataneous depolarization
SAN= 105-110/min which is why it is the pacemaker
Bundle if His= 30-40/min
Mechanism of excitation/contraction coupling
- AP spreads from sarcoplasmic membrane
to T - tubules. - As a result L-type voltage-gated Ca2+
channels open, leading to entry of Ca2+ ions
into sarcoplasm. - Increased concentration of Ca2+ ions in
sarcoplasm induces Ca2+ release from SR by
activation of ryanodine receptor-channels
(RyR) - Ca2+ induced Ca2+ release. - The release of Ca2+ from SR causes Ca2+
spark. - Ca2+ ions bind to troponin to initiate
contraction.
Action of contraction in myocardium
- ATP binds to actinmyosin complex breaking the crossbirges
- ATPase activity of myosin increases
- The ATP molecule is broken down
into ADP and inorganic P. This leads to formation of a new
strong bound between myosin and
actin. - Myosin moves 10 nm towards the M-line of the sarcomere.
- ADP is released, allowing a new ATP molecule to bind to myosin, and the cycle
starts over.
Relaxation in the heart
Ca2+ unbinds from troponin leading to increase in ECF and SR
Ca2+ is pumped back into SR by Ca2+ pump
for storage.
On the cell membrane Ca2+ is exchanged
with Na+ by NCX antiporter.
Na+ gradient is maintained by Na+ - K+
pump.
