CIRCULATORY TRACT
Cardiac cycle –
1. Generate an electrical impulse
2. Conduct the impulse throughout the heart
3. Excitation / contraction coupling
4. Contraction: generate pressure to open valves and eject blood
5. Allow blood to flow back to the heart
Electrical impulses in the heart are generated by the movement of ions across the
cell membrane, a process that is tightly regulated by voltage-gated ion channels.
These channels open and close in response to specific voltage changes in the cell
(depolarization), allowing ions such as sodium (Na⁺), calcium (Ca²⁺), and potassium
(K⁺) to move across the membrane.
Voltage-gated channels are highly selective, meaning they only allow specific ions
to pass through them. For example, sodium channels permit Na⁺ ions, while calcium
channels allow Ca²⁺ ions to move across the membrane. Each type of channel opens
at distinct voltage thresholds. Moreover, these channels vary in their speed of
activation; some open and close rapidly, while others operate more slowly.
The movement of ions across the membrane is
governed by the chemical driving force, which is
determined by the concentration gradient of the
ions. Ions naturally move from areas of high
concentration to areas of lower concentration. In
cardiac cells, there is a high concentration of Na⁺
outside the cell and a lower concentration inside,
which drives Na⁺ to move into the cell when the sodium channels open. Similarly, the
movement of Ca²⁺ is into the cell. The movement of K⁺ is outside the cell. The ions
follows their respective concentration gradients when their channels are activated.
The Nernst potential (ENernst) is the membrane potential at
which the movement of an ion into the cell is balanced by its
movement out. At this point, there is no net movement of that
particular ion, as its inward and outward fluxes are equal.
This allows us to calculate the equilibrium potential for
each ion, based on its concentration gradient. This value tells
us the effect a single ion will have on the overall membrane
potential when its permeability changes, such as when a
specific ion channel opens.
Heart cells –
Specialized cells (conductive system):
• SA node
• AV node
• Bundle of His
• Purkinje fibers
1
,Contractile (muscle) cells = cardiac myocytes:
• Atrial myocytes
• Ventricular myocytes
The heart’s conductive system is made up of specialized cells that have the ability to
generate and conduct electrical impulses, a property known as automaticity.
The process begins with the SA node, located in the right
atrium. Often referred to as the heart’s natural pacemaker, the
SA node generates spontaneous electrical impulses that set
the heart’s rhythm. These impulses spread rapidly through the
atria, causing them to contract and push blood into the
ventricles.
After the atria contract, the electrical impulse reaches the AV
node, situated at the junction between the atria and ventricles.
The AV node has a slower conduction speed, which creates a slight delay before
passing the impulse to the ventricles. This delay is crucial because it allows time for
the ventricles to fully fill with blood from the atria before they contract.
From the AV node, the electrical impulse travels down the Bundle of His, a group of
specialized cells that conduct the impulse from the AV node into the ventricles.
Finally, the electrical impulse is delivered to the Purkinje fibers, which are spread
throughout the ventricles. These fibers ensure that the ventricles contract powerful to
efficiently pump blood out of the heart.
Funny channels are unlike most voltage-gated channels that open in response to
depolarization. Funny channels open when the membrane becomes
hyperpolarized—when the inside of the cell becomes more negative than its resting
potential. When the membrane hyperpolarizes at the end of an action potential, the
funny channels allow sodium ions (Na⁺) to pass into the cell. This gradual influx of
Na⁺ causes the membrane potential to go back toward a more positive value, slowly
depolarizing the cell again and triggering the next action potential. Funny channels
close due to depolarization.
SA node, pacemaker cell –
4: pacemaker potential
• Na+ influx (orange)
• Ca2+ influx T-type (yellow)
0: depolarization
• Ca2+ influx L-type
3: repolarization
• K+ efflux
• Ca2+ channel inactivation
There is a pacemaker potential instead of a resting potential! Also remember that
depolarization is due to Ca2+ instead of Na+.
2
,T-type calcium channels are called "transient" because they open for a short
duration. They are activated at relatively low voltages and contribute to the initial
phase of depolarization in pacemaker cells. L-type calcium channels are referred to
as "long-lasting" because they remain open for a longer period during the action
potential. These channels are activated at higher voltages and are crucial for the
depolarization phase in pacemaker cells.
The autonomic nervous system (ANS)
affects the pacemaker potential.
When the sympathetic nervous system is
activated, it releases noradrenaline and
adrenaline, which bind to beta-adrenergic
receptors on pacemaker cells. This triggers the opening of funny channels (If) and
T-type calcium channels, increasing the influx of sodium (Na⁺) and calcium
(Ca²⁺) ions into the cells. As a result, the membrane potential depolarizes more
quickly. The slope of the pacemaker potential becomes steeper. This means the
heart's electrical system fires more rapidly, leading to an increased heart rate (HR).
• HR
• Contractility ventricles
In contrast, when the parasympathetic nervous system is activated, it releases
acetylcholine (ACh). Acetylcholine binds to muscarinic receptors on pacemaker
cells, reducing the opening of T-type calcium channels and increasing the
opening of potassium (K⁺) channels. This causes more potassium to exit the cell,
leading to hyperpolarization, where the membrane potential becomes more
negative and farther from the threshold for triggering an action potential.
Consequently, the pacemaker potential's slope becomes less steep, and the cell
takes longer to reach the threshold for depolarization. The heart's electrical system
fires less frequently, resulting in a reduced heart rate.
• HR
• Contractility ventricles unaffected
Parasympathetic fibers do not reach the ventricles and can therefore not affect
the contractility. The sympathetic fibers do reach the ventricles and increase the
contractility by Ca2+.
Ventricular muscle cell –
4: resting potential
0: depolarization
• Na+ influx (fast)
1: initial repolarization
• Na+ inactivation
• K+ efflux
3
, 2: plateau
• Ca2+ influx (L-type)
• K+ efflux
3: repolarization
• K+ efflux
• Ca2+ inactivation
In ventricular muscle cells, the resting membrane potential is around -90 mV, which is
very close to the ENernst for K⁺. This means that, at rest, the membrane is primarily
permeable to potassium ions, and there is no hyperpolarization, as the cell is
already at a stable, negative resting potential.
A key feature of ventricular muscle cells is the presence of a plateau phase during
the action potential. The plateau phase prolongs depolarization, which prevents the
generation of a new impulse before the cell has had time to repolarize.
All voltage-gated channels open and close at certain membrane potentials.
After they open during depolarization, both Na⁺ channels and L-type Ca²⁺
channels enter a state of temporary inactivation. This inactivation state of the
channels creates the refractory period, during which the cell is unresponsive to
new stimuli. For the channels to become excitable again, the membrane must
go through repolarization, which restores the resting potential. Repolarization
causes the inactivation gate on these channels to be removed, allowing them to
return to their normal, closed state. Once in this state, the channels are ready to
open again in response to a new action potential.
Tetanus refers to a sustained muscle contraction that occurs when a muscle
receives rapid, repeated stimuli without enough time to relax between each stimulus.
Skeletal muscle –
Rapid successive stimuli can cause a
summation of muscle tension, potentially
leading to tetanus. The refractory period is
short, allowing multiple stimuli to occur in
rapid succession, increasing tension over
time.
Cardiac muscle –
Cardiac muscle is protected from tetanus due
to a long refractory period. This extended
refractory period prevents the muscle from
being re-stimulated too quickly, allowing it to
relax between contractions. This is crucial for
heart function, as it prevents the continuous
contraction that would impair the heart's
ability to pump blood effectively.
4
Cardiac cycle –
1. Generate an electrical impulse
2. Conduct the impulse throughout the heart
3. Excitation / contraction coupling
4. Contraction: generate pressure to open valves and eject blood
5. Allow blood to flow back to the heart
Electrical impulses in the heart are generated by the movement of ions across the
cell membrane, a process that is tightly regulated by voltage-gated ion channels.
These channels open and close in response to specific voltage changes in the cell
(depolarization), allowing ions such as sodium (Na⁺), calcium (Ca²⁺), and potassium
(K⁺) to move across the membrane.
Voltage-gated channels are highly selective, meaning they only allow specific ions
to pass through them. For example, sodium channels permit Na⁺ ions, while calcium
channels allow Ca²⁺ ions to move across the membrane. Each type of channel opens
at distinct voltage thresholds. Moreover, these channels vary in their speed of
activation; some open and close rapidly, while others operate more slowly.
The movement of ions across the membrane is
governed by the chemical driving force, which is
determined by the concentration gradient of the
ions. Ions naturally move from areas of high
concentration to areas of lower concentration. In
cardiac cells, there is a high concentration of Na⁺
outside the cell and a lower concentration inside,
which drives Na⁺ to move into the cell when the sodium channels open. Similarly, the
movement of Ca²⁺ is into the cell. The movement of K⁺ is outside the cell. The ions
follows their respective concentration gradients when their channels are activated.
The Nernst potential (ENernst) is the membrane potential at
which the movement of an ion into the cell is balanced by its
movement out. At this point, there is no net movement of that
particular ion, as its inward and outward fluxes are equal.
This allows us to calculate the equilibrium potential for
each ion, based on its concentration gradient. This value tells
us the effect a single ion will have on the overall membrane
potential when its permeability changes, such as when a
specific ion channel opens.
Heart cells –
Specialized cells (conductive system):
• SA node
• AV node
• Bundle of His
• Purkinje fibers
1
,Contractile (muscle) cells = cardiac myocytes:
• Atrial myocytes
• Ventricular myocytes
The heart’s conductive system is made up of specialized cells that have the ability to
generate and conduct electrical impulses, a property known as automaticity.
The process begins with the SA node, located in the right
atrium. Often referred to as the heart’s natural pacemaker, the
SA node generates spontaneous electrical impulses that set
the heart’s rhythm. These impulses spread rapidly through the
atria, causing them to contract and push blood into the
ventricles.
After the atria contract, the electrical impulse reaches the AV
node, situated at the junction between the atria and ventricles.
The AV node has a slower conduction speed, which creates a slight delay before
passing the impulse to the ventricles. This delay is crucial because it allows time for
the ventricles to fully fill with blood from the atria before they contract.
From the AV node, the electrical impulse travels down the Bundle of His, a group of
specialized cells that conduct the impulse from the AV node into the ventricles.
Finally, the electrical impulse is delivered to the Purkinje fibers, which are spread
throughout the ventricles. These fibers ensure that the ventricles contract powerful to
efficiently pump blood out of the heart.
Funny channels are unlike most voltage-gated channels that open in response to
depolarization. Funny channels open when the membrane becomes
hyperpolarized—when the inside of the cell becomes more negative than its resting
potential. When the membrane hyperpolarizes at the end of an action potential, the
funny channels allow sodium ions (Na⁺) to pass into the cell. This gradual influx of
Na⁺ causes the membrane potential to go back toward a more positive value, slowly
depolarizing the cell again and triggering the next action potential. Funny channels
close due to depolarization.
SA node, pacemaker cell –
4: pacemaker potential
• Na+ influx (orange)
• Ca2+ influx T-type (yellow)
0: depolarization
• Ca2+ influx L-type
3: repolarization
• K+ efflux
• Ca2+ channel inactivation
There is a pacemaker potential instead of a resting potential! Also remember that
depolarization is due to Ca2+ instead of Na+.
2
,T-type calcium channels are called "transient" because they open for a short
duration. They are activated at relatively low voltages and contribute to the initial
phase of depolarization in pacemaker cells. L-type calcium channels are referred to
as "long-lasting" because they remain open for a longer period during the action
potential. These channels are activated at higher voltages and are crucial for the
depolarization phase in pacemaker cells.
The autonomic nervous system (ANS)
affects the pacemaker potential.
When the sympathetic nervous system is
activated, it releases noradrenaline and
adrenaline, which bind to beta-adrenergic
receptors on pacemaker cells. This triggers the opening of funny channels (If) and
T-type calcium channels, increasing the influx of sodium (Na⁺) and calcium
(Ca²⁺) ions into the cells. As a result, the membrane potential depolarizes more
quickly. The slope of the pacemaker potential becomes steeper. This means the
heart's electrical system fires more rapidly, leading to an increased heart rate (HR).
• HR
• Contractility ventricles
In contrast, when the parasympathetic nervous system is activated, it releases
acetylcholine (ACh). Acetylcholine binds to muscarinic receptors on pacemaker
cells, reducing the opening of T-type calcium channels and increasing the
opening of potassium (K⁺) channels. This causes more potassium to exit the cell,
leading to hyperpolarization, where the membrane potential becomes more
negative and farther from the threshold for triggering an action potential.
Consequently, the pacemaker potential's slope becomes less steep, and the cell
takes longer to reach the threshold for depolarization. The heart's electrical system
fires less frequently, resulting in a reduced heart rate.
• HR
• Contractility ventricles unaffected
Parasympathetic fibers do not reach the ventricles and can therefore not affect
the contractility. The sympathetic fibers do reach the ventricles and increase the
contractility by Ca2+.
Ventricular muscle cell –
4: resting potential
0: depolarization
• Na+ influx (fast)
1: initial repolarization
• Na+ inactivation
• K+ efflux
3
, 2: plateau
• Ca2+ influx (L-type)
• K+ efflux
3: repolarization
• K+ efflux
• Ca2+ inactivation
In ventricular muscle cells, the resting membrane potential is around -90 mV, which is
very close to the ENernst for K⁺. This means that, at rest, the membrane is primarily
permeable to potassium ions, and there is no hyperpolarization, as the cell is
already at a stable, negative resting potential.
A key feature of ventricular muscle cells is the presence of a plateau phase during
the action potential. The plateau phase prolongs depolarization, which prevents the
generation of a new impulse before the cell has had time to repolarize.
All voltage-gated channels open and close at certain membrane potentials.
After they open during depolarization, both Na⁺ channels and L-type Ca²⁺
channels enter a state of temporary inactivation. This inactivation state of the
channels creates the refractory period, during which the cell is unresponsive to
new stimuli. For the channels to become excitable again, the membrane must
go through repolarization, which restores the resting potential. Repolarization
causes the inactivation gate on these channels to be removed, allowing them to
return to their normal, closed state. Once in this state, the channels are ready to
open again in response to a new action potential.
Tetanus refers to a sustained muscle contraction that occurs when a muscle
receives rapid, repeated stimuli without enough time to relax between each stimulus.
Skeletal muscle –
Rapid successive stimuli can cause a
summation of muscle tension, potentially
leading to tetanus. The refractory period is
short, allowing multiple stimuli to occur in
rapid succession, increasing tension over
time.
Cardiac muscle –
Cardiac muscle is protected from tetanus due
to a long refractory period. This extended
refractory period prevents the muscle from
being re-stimulated too quickly, allowing it to
relax between contractions. This is crucial for
heart function, as it prevents the continuous
contraction that would impair the heart's
ability to pump blood effectively.
4
