Transcript Zool 352 Lecture 33

Cardiac Muscle I
Essential Features of Vertebrate
Cardiac Muscle
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Striated
Cells connected by gap junctions
Dually innervated by ANS
Spontaneously active, either normally or in
disease states, depending on the cell type.
• In mammals: highly dependent on
oxidative metabolism
Differentiation of Functional Cell Types
in the Heart
• Nodal fibers- spontaneously active
pacemakers that can initiate heartbeat
• Conducting fibers - rapidly carry
excitation from one part of the heart to
another
• Myocardial fibers - compose most of the
mass of the heart and provide essentially
all of the force.
Nodal and conducting fibers in the heart
Sequence of electromechanical
events in a heartbeat
• Spontaneous AP in SA nodal
pacemakers
• Excitation spreads throughout atria,
followed by atrial contraction
• Excitation reaches AV node, enters
bundle of His, is conducted into both
ventricles by branch bundles, and is
rapidly spread throughout the
ventricular myocardium by Purkinjie
fibers - followed by ventricular
Agenda of topics to consider
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Nature of pacemaker action potentials
Control of heart rate by the ANS
Nature of myocardial action potentials
Relationship between myocardial action
potentials and the electrocardiogram
• Myocardial excitation-contraction
coupling
• Control of myocardial contractile force
by stretch and by autonomic inputs
Action potentials
recorded from the
ventricular
myocardium, SA
node and atrial
myocardium.
The total time in
each window is
about 300 msec
for the
myocardial cells
and about 150
msec for the SA
nodal cell.
Pacemaker potentials
• Nodal cells (pacemakers) do not have
stable resting potentials.
• Instead, the cells undergo a
spontaneous, slow depolarization
(prepotential) until threshold is reached.
• The upstroke of the AP is slow
compared to nerve and skeletal muscle.
• Each action potential leads to a
temporary afterhyperpolarization that
leads into the next prepotential.
If inward
K+
T Ca++
L Ca++
The rate of pacemaker potentials is
modulated by the autonomic NS
• In the absence of any autonomic input, the
natural rate of pacemaker potentials is
about 100/min in human heart.
• Cholinergic input slows the heart rate by
slowing depolarization during the
prepotential; adrenergic input increases
the heart rate by increasing the rate of
depolarization.
This slide shows the effects of isoproterenol (a beta agonist;
A), stimulation of the vagus nerve (B), and two concentrations
of Ach. Before and after traces are overlain; c indicates
control beats and * experimental beats.
How beta1 receptors increase heart
rate
• Second messenger: cAMP (slow), but
directly by Gs (rapid)
• Channel effects:
• 1. shift activation of L channels to more
negative voltages, causing threshold to
be reached sooner; increase current
carried by L channels.
• 2. Increase If, causing hypolarization at
beginning of prepotential to be smaller.
How muscarinic receptors slow the
heart
• Second messengers: Gi-mediated
inhibition of adenylyl cyclase (slow); but
direct effect of Gi on K+ channels (rapid).
• Channel effects:
• 1. Open Ach-sensitive K+ channels
• 2. Shift L channel activation to more
positive voltage values and decrease
channel conductance.
• 3. Decrease If, causing a greater
hyperpolarization at the beginning of the
prepotential.
Key features of the myocardial action
potential
• Rapid upstroke
• LONG plateau
• Potential relatively stable during the
interbeat interval, except in disease.
Channels involved in the myocardial AP
“fast” Na+ channels
L Ca++ channels
K+ channels
(several types)
The electrocardiogram is an
extracellular recording of the
myocardial AP
• Voltage is measured at several spots on
the body surface - because body fluid is
a conductor of electricity, these spots
could be thought of as wires connected
directly to the heart surface.
• A voltage difference will exist only when
some parts of the heart are depolarized
while others are not. During the
interbeat interval, OR when the ventricle
is all depolarized, the EKG trace will
return to baseline.
If we measure the voltage difference
between the right arm and left leg
over a heart cycle, we will watch
excitation start in the atria, spread
through the ventricles, and end with
ventricular repolarization
Relationship between atrial and ventricular AP s and EKG
waves
Atrial
Ventricular