SMOOTH

MUSCLE
• Smooth muscle lacks striations, which differs it
from skeletal and cardiac muscle.
• The striations of skeletal and cardiac muscle are
created by the bands of thick and thin filaments in
the sarcomeres.
• In smooth muscle, there are no striations because
the thick and thin filaments are not organized in
sarcomeres.
Contraction of Smooth Muscle
• In contrast, skeletal muscle fibers are as much as 30 times greater
in diameter and hundreds of times as long.
• Many of the same principles of contraction apply to smooth
muscle as to skeletal muscle.
• Most important, the same attractive forces between myosin and
actin filaments cause contraction in smooth muscle as in skeletal
muscle.
• Smooth muscle is found in
the walls of hollow organs:
the gastrointestinal tract, the
bladder, the uterus, in the
vasculature, the ureters, the
bronchioles, and the
muscles of the eye.
• The functions of smooth
muscle are twofold: to
produce motility and to
maintain tension (e.g.,
smooth muscle in the walls
of blood vessels).
Types of Smooth Muscle

• The smooth muscle of each organ is different from that

of most other organs in several ways:
• (1) physical dimensions,
• (2) organization into bundles or sheets,
• (3) response to different types of stimuli, (4)
characteristics of innervation, and
• (5) function.
• smooth muscle can generally be divided into two major
types: multi-unit smooth muscle and unitary (or single-
unit) smooth muscle.
 TYPES OF SMOOTH MUSCLES
A third type, a
combination of unitary
Smooth muscles and multiunit smooth
muscle

vascular smooth
unitary
multiunit muscle.

has gap junctions

between cells, which
allow for the fast has little or no
spread of electrical coupling between cells
activity throughout the
organ
Unitary Smooth Muscle

• Unitary (single unit) smooth muscle is present in the
gastrointestinal tract, bladder, uterus, and ureter.
• The smooth muscle in these organs contracts in a
coordinated manner because the cells are linked by gap
junctions.
• Gap junctions are low-resistance pathways for current flow.
• Action potentials occur simultaneously in the smooth
muscle cells of the bladder so that contraction (and
emptying) of the entire organ can occur at once.
Unitary Smooth Muscle
• This type of smooth muscle is known as syncytial
smooth muscle because of its syncytial
interconnections among fibers.
• It is also called visceral smooth muscle because it
is found in the walls of most viscera of the body,
including the gastrointestinal tract, bile ducts,
ureters, uterus, and many blood vessels.
Unitary Smooth Muscle
• Unitary smooth muscle is also characterized by
spontaneous pacemaker activity, or slow waves.
• The frequency of slow waves sets a characteristic
pattern of action potentials within an organ, which
then determines the frequency of contractions.
Multi-Unit Smooth Muscle
• This type is composed of discrete, separate smooth
muscle fibers.
• Each fiber works independently of the others and often is
innervated by a single nerve ending, as skeletal muscle
fibers.
• the outer surfaces of these fibers, like skeletal muscle
fibers, are covered by a thin layer of basement membrane-
like substance, a mixture of fine collagen and glycoprotein
that helps insulate the separate fibers from one another.
Multi-Unit Smooth Muscle
• Multiunit smooth muscle is present in the iris, in the ciliary muscles of
the lens, and in the vas deferens.
• Each muscle fiber can act as a separate motor unit (similar to skeletal
muscle), and there is little or no coupling between cells.
• The most important characteristic is that each fiber can contract
independently of the others,
• and their control is exerted mainly by nerve signals.
Multi-Unit Smooth Muscle
• Multiunit smooth muscle cells are
innervated by postganglionic fibers of the
parasympathetic and sympathetic nervous
systems.
EXCITATION-
CONTRACTION
COUPLING IN
SMOOTH MUSCLE
Chemical Basis for Smooth Muscle Contraction
• Smooth muscle contains both actin and myosin filaments with
chemical characteristics similar to those of the actin and myosin
filaments in skeletal muscle.
• It does not contain the troponin complex, so the mechanism for
control of contraction is different.
• actin and myosin filaments interact with each other in the same
way that they do in skeletal muscle.
• the contractile process is activated by Ca2+,
• ATP is degraded to (ADP) to provide the energy for contraction.
Chemical Basis for Smooth Muscle Contraction

but there are major differences between the

physical organization of smooth muscle and
that of skeletal muscle, as well as
• differences in excitation-contraction
coupling,
• control of the contractile process by Ca2+,
• duration of contraction,
• and amount of E required
for contraction.
Physical Basis for Smooth Muscle Contraction

• Smooth muscle does not have the
striated arrangement as skeletal
muscles.
• There are large numbers of actin
filaments attached to so-called
dense bodies.
• Some of these bodies are attached
to the cell membrane.
• Others are dispersed inside the cell.
• Some of the dense bodies of
adjacent cells are bonded together
by intercellular protein bridges.
through these bonds that the force
of contraction is transmitted from
one cell to the next.
Physical Basis for Smooth Muscle Contraction
• We can see large numbers
of actin filaments radiating
from two dense bodies;
• the ends of these filaments
overlap a myosin filament
located midway between
the dense bodies.
• the dense bodies of smooth
muscle serve the same role
as the Z discs
Slow Cycling of the Myosin Cross-Bridges
• The rapidity of cycling of the myosin cross-bridges
in smooth muscle-that is, their attachment to actin,
then release from the actin, and reattachment for
the next cycle-is much slower than in skeletal
muscle;
• the time that the cross-bridges remain attached to
the actin filaments is greatly increased in smooth
muscle.
• A possible reason for the slow cycling is that the
cross-bridge heads have far less ATPase activity
than in skeletal muscle
Low Energy Requirement to Sustain Smooth Muscle
Contraction

• The smooth muscle is required far less E to
sustain the same tension of contraction
than in skeletal muscle.
 Slowness of Onset of Contraction and Relaxation

• A typical smooth muscle tissue begins to contract 50 to 100
milliseconds after it is excited, reaches full contraction
about 0.5 second later, and then declines in contractile force
in another 1 to 2 seconds, giving a total contraction time of
1 to 3 seconds.
• This is about 30 times as long as a single contraction of
skeletal muscle fiber.
• The slow onset of contraction of smooth muscle, its
prolonged contraction, is caused by the slowness of
attachment and detachment of the cross-bridges with the
actin filaments.
• In addition, the initiation of contraction in
response to Ca2+ is much slower than in
skeletal muscle.
Maximum Force of Contraction Is Often Greater in Smooth Muscle
Than in Skeletal Muscle

• Despite the few myosin filaments in smooth

muscle, and despite the slow cycling time of the
cross-bridges, the maximum force of contraction
of smooth muscle is often greater than that of
skeletal muscle.
• This great force of smooth muscle contraction
results from the prolonged period of attachment of
the myosin cross-bridges to the actin filaments.
Regulation of Contraction by Calcium Ions

• the initiating stimulus for most smooth muscle contraction
is an increase in intracellular Ca2+.
• This increase can be caused in different types of smooth
muscle by
• nerve stimulation of the smooth muscle fiber,
• hormonal stimulation,
• stretch of the fiber,
• or even change in the chemical environment of the fiber.
• But smooth muscle does not contain troponin.
• Instead, smooth muscle contraction is activated by
an entirely different mechanism, as follows -
Ca2+ Combine with Calmodulin to Cause Activation of
Myosin Kinase and Phosphorylation of the Myosin Head

• Instead of troponin, smooth muscle cells contain a

large amount of calmodulin.
• Although this protein is similar to troponin, it is
different in the manner in which it initiates
contraction.
• Calmodulin does this by
activating the myosin
cross-bridges.
• This activation and
contraction
occur in the following
sequence:
• The mechanism of excitation-contraction coupling in
smooth muscle differs from that of skeletal muscle.
• In skeletal muscle binding of actin and myosin is occurred
when Ca2+ binds troponin C.
• In smooth muscle there is no troponin.
• The interaction of actin and myosin is controlled by the
binding of Ca2+ to another protein, calmodulin.
• In turn, Ca2+-calmodulin regulates myosin-light-chain
kinase, which regulates cross-bridge cycling.
Steps in Excitation-Contraction Coupling in
Smooth Muscle
1.
Action potentials occur in the
smooth muscle cell membrane.

The depolarization of smooth

muscle opens voltage-gated Ca2+
channels in the sarcolemma.

Ca2+ flows into the cell down its

electrochemical gradient.

Influx of Ca2+ from the ECF causes

an increase in intracellular Ca2+
concentration.
In contrast to sceletal muscle, where AP are required for contraction,
in smooth muscle, subthreshold depolarisation can open these
voltage-gated Ca2+channels and cause increasing intracellular
Ca2+concentration.

If the depolarisation of smooth muscle membrane reaches

threshhold, then AP can occur, causing greater depolarisation and
greater opening of voltage-gated Ca2+ channels.

Ca2_ that enters the smooth muscle cells through voltage-gated

Ca2+ releases additional Ca2- from SR (Ca2+-induced release).

So the rise in intracellular Ca2+ is partly due to Ca2+ entry across

sarcolemma and partly due to Ca2+ release from SR.
 Ligand-gated Ca2+
channels in the
2.
sarcolemma can opened
Two additional by various hormones and
mechanisms may neurotransmitters,
contribute to the causing the entry of
increase in intracellular additional Ca2+ from the
Ca2+ concentration: ECF.
ligand-gated Ca2+ IP3-gated Ca2+ release
channels and inositol channels in the
1,4,5-triphosphate (IP3)- membrane of the
gated Ca2+ release sarcoplasmic reticulum
channels. can be opened by
. hormones and
neurotransmitters.
3. Ca2+ bind to calmodulin. Like troponin
C in skeletal muscle, calmodulin binds 4
ions of Ca2+.
The Ca2+-calmodulin complex binds to
and activates myosin-light-chain kinase.
 • When activated, myosin-
4. light-chain kinase
phosphorylates myosin.
• When myosin is
phosphorylated, it binds
actin to form cross-
bridges and production of
tension.
• Amount of tension is
proportional to
intracellular Ca2+
concentration.
5.

Ca2+-calmodulin also has effects on 2 thin filament proteins,

calponin and caldesmon.

At low levels intracellular Ca2+ they bind actin, inhibiting

myosin ATP-ase and preventing interaction betweeen actin and
myosin.

When intracellular Ca2+ increases, Ca2+calmodulin complex

leads to phosphorylation of calponin and caldesmon, releasing
their inhibition of ATP ase and facilitate formation of cross-
bridges.
 6. RELAXATION
• When the intracellular Ca2+ concentration decreases,
• myosin is dephosphorylated by myosin-light-chain phosphatase.
• In the dephosphorylated state, myosin can still interact with actin,
but the attachments are called latch-bridges rather than cross-
bridges.
• The latch-bridges do not detach, or they detach slowly;
• thus, they maintain a tonic level of tension in the smooth muscle
with little consumption of ATP.
6.

Relaxation occurs when the

sarcoplasmic reticulum reaccumulates
Ca2+, via the Ca2+ ATPase,

and lowers the intracellular Ca2+

concentration below the level
necessary to form Ca2+-calmodulin
complexes.
Mechanisms That Increase Intracellular
Ca2+ Concentration in Smooth Muscle
1) During the action potential in smooth muscle,
Ca2+ enters the cell from ECF via voltage-gated
Ca2+ channels, which are opened by depolarization.

2) Ca2+ can enter the cell through ligand-gated

channels

3) or it can be released from the sarcoplasmic

reticulum by IP3-gated mechanisms.
Voltage-gated Ca2+ channels
• are sarcolemmal Ca2+ channels that open when
the cell membrane potential depolarizes.

action potentials in the smooth muscle cell

membrane cause voltage-gated Ca2+ channels to
open,

allowing Ca2+ to flow into the cell down its

electrochemical potential gradient.
Ligand-gated Ca2+ channels

also are present in the sarcolemmal membrane.

Various hormones and neurotransmitters interact with

specific receptors in the sarcolemmal membrane,
which are coupled via a GTP-binding protein (G protein)
to the Ca2+ channels.

When the channel is open, Ca2+ flows into the cell

down its electrochemical gradient.
IP3-gated sarcoplasmic reticulum Ca2+
channels

also are opened by hormones and neurotransmitters.

The source of the Ca2+ is the sarcoplasmic reticulum.

Hormones or neurotransmitters interact with specific receptors on the

sarcolemmal membrane (e.g., norepinephrine with α1 receptors).

These receptors are coupled, via a G protein, to phospholipase C (PLC).

Phospholipase C catalyzes the hydrolysis of phosphatidylinositol 4,5-diphosphate

(PIP2) to IP3 and diacylglycerol (DAG).

IP3 then diffuses to the sarcoplasmic reticulum, where it opens Ca2+ release
channels. Ca2+ flows from its storage site in the sarcoplasmic reticulum into the
ICF.
Nervous Control of Smooth Muscle Contraction

• Although skeletal muscle fibers are stimulated by the
nervous system, smooth muscle can be stimulated to
contract by multiple types of signals:
by nervous signals,
by hormonal stimulation,
by stretch of the muscle,
and in several other ways.
The principal reason for the difference is that the smooth
muscle membrane contains many types of receptor
proteins that can initiate the contractile process.
Still other receptor proteins inhibit smooth muscle
contraction, which is another difference from skeletal
muscle.