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Physiology 2a
CVS 1:
Cardiac and smooth muscle
David Saint
Discipline of Physiology

Phys 2: CVS overall

Assumed knowledge
A knowledge of the basic anatomy of the heart
(chambers, valves, etc)
A knowledge of the basic layout of the circulation
(systemic and pulmonary)
Basic chemistry: ions, aqueous solutions,
concentrations (moles), lipids, proteins, etc
Basic physics: A basic understanding of pressure
and flow, and the units used to measure them. A
basic understanding of electrical circuits, Ohms
law.

Phys 2: CVS 1: Learning objectives

An understanding of the differences and
similarities between skeletal and cardiac muscle
in the triggering and control of contraction
An understanding of the Frank-Starling relation
and its importance in controlling cardiac output
An understanding of the mechanism of contraction
in smooth muscles
An appreciation that smooth muscle lacks a length
tension relation, and the physiological importance
of this

Cardiac muscle

Cardiac muscle is striated

forms a syncitium (all one network)
involuntary
mechanism of contraction is similar to skeletal
muscle (involves tropomyosin)
source of calcium for contraction is similar to
skeletal muscle, but release mechanism is different
neural control of contraction is different from skeletal
muscle

Structure of heart muscle

Arrangement of
sarcomeres
and contractile
proteins is
essentially the
same as in
skeletal muscle.

Cardiac muscle contraction:

actin-myosin interaction
Ca++
Ca++

DAS

Cross bridge cycling

Take- home message: requires ATP

Where does the calcium come from?

The
sarcoplasmic
reticulum is an
internal calcium
store
Calcium release
is triggered by
extracellular
calcium
entering the cell
through L-type
calcium
channels.

What causes the calcium influx?

Opening of L-type calcium channels
(equivalent of DHP receptors in skeletal)
during the plateau phase of the action
potential allows calcium to flow down its
electrochemical gradient
(Ca++ inside the cells is normally very low:
Ca++ outside is about 1.5 mM)

What causes the Ca++ release?

In skeletal muscle
there is thought to
be a direct
mechanical
coupling between
the DHP receptors
and the calcium
release channels

Calcium-induced calcium release

Ca++

In cardiac muscle,
there is no such
direct linkThe coupling
between the DHP
receptors and the
calcium release
channels is by
calcium influx
itself!

Calcium-induced calcium release

Ca++

Ca++

In cardiac
muscle, the DHP
receptors
actually are
voltage gated
calcium
channels (Ltype) and allow
calcium influx

Calcium-induced calcium release

Ca++

Ca++

The rise in internal

calcium allows
calcium to bind to a
site on the
RyR receptors
(calcium release
channels)
and they open,
allowing calcium
release

Cardiac muscle:
timing and control of contraction
skeletal muscle
AP

cardiac muscle
contraction

contraction

AP

DAS

potential

Cardiac muscle:
ventricular action
potential

time (sec)

Notethatsympatheticns
affectsthecalciumcurrent:
Increasingforceofcontraction

potassium current

relative permeability

sodium current

calcium current

Cardiac muscle:
control of contraction
cant get a tetanus in cardiac muscle
(because of long action potential)
no such thing as motor units
(because its a syncitium)
neuronal input modulates contraction,
(force and rate) but doesnt initiate it

Control of stroke volume:

Frank-Starling law
The output of the heart has to match the
input and the two sides have to match
each other.
The Frank-Starling law states that the force
of contraction of the heart (blood pumped
out) increases when the end-diastolic
pressure and volume is increased (ie
muscle is stretched)

Why is it
important?

Note:
Two separate loops, pulmonary
and vascular circulation. Note
that the same volume of blood
per second flows through each
circuit.
The heart is a dual pump
(although both sides contract at
the same time)
The output of the two sides has
to balance

tension

Muscle contraction:
length tension curve (skeletal)

resting length

Length-tension relation
in the heart

Tension
(force of
contraction)

increase in filling
pressure results in
increased output

resting length (determined by filling pressure)

Control of stroke volume

Heart failure

Cardiac muscle: Summary

Mechanism of contraction is the same
(actin and myosin, sarcomeres, troponin, etc)
Source of calcium is similar
(mostly from internal stores, as opposed to entirely from stores)
Triggering of calcium release is different (CICR)
Control of tension is different (action potential duration)
Length tension curve is different (no descending limb)
Frank-Starling law is important to match pulmonary and
systemic outputs

Smooth muscle
not striated (thats why its called smooth!)
no clear length / tension relationship
mechanism of contraction is different from
cardiac and skeletal (no troponin)
contraction depends on extracellular calcium
almost exclusively
no 1:1 relation between tension and action
potentials
can have lots of tone

Smooth muscle:
mechanism of contraction
contracted

relaxed

thick filament

thin filament
dense body
DAS

Smooth muscle
mechanism of contraction
Ca++
Ca++ calmodulin

Calmodulin

Inactive myosin
Kinase

Active myosin
Kinase

Pi
Inactive Myosin
DAS

Phosphorylated
Myosin

Smooth muscle:
control of contraction

pacemaker potential

slow wave potential

Muscle types: overview

skeletal

smooth
(single unit)

cardiac

smooth
(multi unit)