Samenvatting
Summary Circulatory tract lectures
Samenvatting Circulatory tract
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Voorbeeld van de inhoud
Circulatory tractIntroduction lecture Hoeke Baarsma
The cardiovascular system:
The heart rhythm has 5 phases:
1. Late diastole (the phase during which the heart relaxes and
fills again with blood): both chambers are relaxed and
ventricles fill passively.
2. Atrial systole (phase during which the heart’s atria/ventricles
contract): atrial contraction forces a small amount of additional
blood into ventricles
3. Isovolumic ventricular contraction (volume remains the same):
first phase of ventricular contraction pushes AV valves closed
but does not create enough pressure to open semilunar valves
4. Ventricular ejection: as ventricular pressure rises and exceeds
pressure in the arteries, the semilunar valves open and blood
is ejected.
5. Isovolumetric ventricular relaxation: as ventricles relax, pressure in
ventricles falls, blood flows back into cups of semilunar valves and snaps
them close.
Depolarization of autorhythmic cells in the SA (sinoatrial) node rapidly spread to
adjacent contractile cells (cardiomyocytes) through gap junctions. If SA node is
damaged, slower pacemaker cells (cardiocytes) take over (AV node).
Electrical conduction in the heart:
1. SA node depolarizes
2. Electrical activity goes rapidly to AV node via internodal pathways
3. Depolarization spreads more slowly across the atria. Conduction slows
through the AV node
4. Depolarization moves rapidly through ventricular
conducing system to the apex of the heart.
5. Depolarization wave spreads upward from the apex.
Delay in the AV-nodes lead to atria emptying before
ventricular contraction. The AV-bundle is the Bundle of His.
Refractory period: after an action potential initiates, the
cardiac cell is unable to initiate another action potential for
some duration of time. This period of time is referred to as
the refractory period, which is ~250ms in duration and helps
to protect the heart.
,Action potential of skeletal muscle depends on somatic motor neuron which release ACh at
neuromuscular junction. Net entry of Na+ through ACh receptor-channel initiates a muscle
action potential. This is a voluntary control, via neurons, not via hormones. The action
potential opens DHP channels > opens the RyR channels > Ca+ release from the
sarcoplasmic reticulum > myosin/actin activation and contraction.
The resting potential of pacemaker cells is -60mV, and the threshold -40mV. This is due to
‘funny channels’, which are only present on pacemaker cells. The pacemaker potential
(-60mV to -40mV): Na+ influx by funny channels If > action potential: influx of Ca2+
The contractile cells have a resting potential of -90mV, and a threshold of -70mV.
The plateau phase of the contractile myocytes is 200ms.
Action potential of contractile (myocyte) cells:
Muscle cells
- Skeletal muscle: large fibers, multinucleate cells that appear striped or striated
- Cardiac muscle: straited but smaller, branched, uninucleate. Cells are joined in series
by junctions called intercalated disks
- Smooth muscle: fibers are small and lack striations
Microfibril: bundle of contractile and elastic proteins
Sarcomere: interaction between myosin and actin
Skeletal muscle cell contraction:
In the relaxed state, myosin heads is cocked. Tropomyosin
partially blocks binding site on actin. Myosin is weakly bound to
actin. Initiation of contraction > Ca2+ levels increase > Ca2+
binds to troponin > tropomyosin gets pulled away from actin’s-
myosin binding site > myosin binds strongly to actin and
completes power stroke > actin filament moves. No bound ATP
or ADP > rigor mortis.
,Smooth muscle contraction:
Intermediate filaments and protein dense bodies form a
cytoskeleton. Actin attaches to the dense bodies. Each
myosin molecule is surrounded by actin filaments. Smooth
muscles do not contain troponin. There are no sarcomeres,
and have a slow contraction compared to skeletal muscles.
Excitation-contraction coupling:
Induced by Ca2+ derived from ECF due to stretch, pacemaker activity (ion
channels), or electrical stimulation, or by activation of M3 > Gq > PLC >
IP3 > release of Ca2+ from sarcoplasmic reticulum. Ca2+ binds Ca2+-
calmodulin > complex > activates MLCK > activates myosin (ATP) >
increased muscle tension. Relaxation by inhibition of MLCK or activation of
MLC phosphatase (dephosphorylation).
Cardiac muscle cells:
Striated muscle tissue, sarcomeres present, one nucleus per cell.
Contraction induced by Ca2+. Desmosomes regulate cell-cell contact, gap
junctions regulate transmission of signal to/from neighbouring cells, and
the T-tubule regulates conduction of AP.
L-type Ca2+ channel.
Comparison – control:
- Skeletal: Ca2+ and troponin, fibers
independent of one another
- Smooth: Ca2+ and calmodulin, some fibres
electrically linked via gap junction, others
independent
- Cardiac: Ca2+ and troponin, fibres
electrically linked via gap junctions
, Autonomic nervous system:
The heart is autonomic because of autorhythmic cells, but is regulated by the autonomic NS.
The autonomic NS does not generate an action potential; however it does have an effect on
the heart’s frequency, beating strength, and conduction.
Sympathetic nervous system – heart rate
Sympathetic stimulation and epinephrine depolarize the autorhythmic cell and speed up the
depolarization rate, increasing the heart rate. The contractile force can also be increased by
sympathetic stimulation. Gs activation > adenylyl cyclase > cAMP > PKA > influences Ca2+.
The heart has both β1 and β2 adrenoceptors, although mainly β1, Gs coupled.
Enhanced inotropy (strength of heartbeat):
- Phosphorylation of L-type Ca2+ channels by PKA > Ca2+ influx > enhanced release
of Ca2+ from SR
- PKA > enhanced release of Ca2+ from RyR-receptors > more Ca2+ for binding the
troponin
- PKA > phosphorylation myosin light chains
- Gs coupled activation increases heart rate by opening ion channels responsible for
pacemaker currents in the SA node
Chronotropic = increased beating rate. Possible adverse effects are that the heart’s O2
consumption increases.
Parasympathetic nervous system – heart rate
Parasympathetic stimulation hyperpolarizes the membrane potential of the autorhythmic cell
and slows depolarization, decreasing the heart rate. This is done by an increase in K+
permeability, and a reduced Ca2+ permeability. The M2 receptor is the main receptor for the
parasympathetic nervous system. They are mainly found on the atria and pacemaker cells.
M2 receptor > Gi > inactivated adenylyl-cyclase > less cAMP > funny channels reduce Ca2+.
Negative dromotropic effect = reduced AV node conduction.
Agonist: acetylcholine
Antagonist: atropine
β1/2
M2
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