Smooth muscle lacks coarse connective tissue sheaths such as are found in the skeletal muscle.
Smooth Muscle
Smooth muscle lacks coarse
connective tissue sheaths such as are found in the skeletal muscle. Most smooth
muscle is made up of sheets of fibers that are closely apposed, such as in the
walls of all except the smallest blood vessels and in the walls of hollow
organs of var-ious systems. Usually, there are two sheets of smooth muscle,
with their fibers situated at right angles to each other. In a smooth muscle’s longitudinal layer, fibers run parallel
to the long axis of the organ. When these fibers contract, the organ shortens.
In a circular layer, fibers are located around the organ’s circumference. When
this layer contracts, the lumen of the organ con-stricts. Alterations of
contraction and relaxation result in peristalsis. Examples of such smooth
muscle action include the rectum, urinary bladder, uterus, lungs, and stomach.
The thin filaments of smooth
muscle have no troponin complex. There are more thin filaments than thick
filaments. However, the thick and thin fil-aments are arranged diagonally.
Smooth muscles lack sarcomeres because there are no striations. There is an
intermediate filament dense body network. These intermediate filaments resist
tension. Dense bodies are also attached to the sarcolemma, anchoring thin fil-aments. These
dense bodies correspond to the Z discs found in skeletal muscle. In smooth
muscle sarco-plasm, calcium ions interact with calmodulin, which is a calcium-binding protein that activates the enzyme myosin kinase. This enables myosin heads to attach
to actin. Stretched smooth muscles
adapt to their new lengths and remain able to contract on demand, a con-dition
known as plasticity.
In the digestive tract, pacesetter cells
spon-taneously trigger contraction of entire sheets of muscle. They are also
called pacemaker cells. When excited,
they set the pace of contraction for the entire muscle sheet. The membrane
potentials of these cells fluctuate and are self -excitatory. In the absence of
external stimuli, they depolarize spontaneously. The rate and intensity of
smooth muscle contraction can, however, be modified by both neural and chemical
stimuli.
In smooth muscles, innervating
nerve fibers exist, which are part of the autonomic (involuntary) nervous
system. They have many bulb-like swellings called varicosities, which release neurotransmitters into a wide synaptic cleft near smooth
muscle cells. These are known as diffuse
junctions. The sarco-lemma of smooth
muscles has many caveolae, which are pouch-like infoldings. The caveolae contain some
extracellular fluid with a high concentration of cal-cium ions near the
membrane. T-tubules are absent in smooth muscle. When calcium channels open in
the caveolae, calcium ion influx occurs quickly. Most of these ions enter
through calcium channels directly from the extracellular space. When
cytoplasmic cal-cium is actively transported into the SR and out of the cell,
contraction ends.
Myoblasts are the embryonic mesoderm cells
from which most muscle tissue develops.
Develop-ment occurs quickly, with the embryo experiencing skeletal muscle fiber
contraction by week 7. The sur-faces of developing myoblasts are initially
covered with ACh receptors. Spinal nerves eventually penetrate the muscle
masses. Nerve endings seek out individual myoblasts and release agrin, a growth factor. Agrin activates MuSK, a muscle kinase. This stimulates
clus-ters of ACh receptors at new neuromuscular junctions and maintains them in
each muscle fiber. The nerve endings release another chemical to eliminate
recep-tor sites that have not been innervated or stabilized by the released
agrin.
Smooth muscle contraction is
similar to that of skeletal muscle, using actin, myosin, calcium ions, and ATP;
however, smooth muscle is also affected by another
neurotransmitter—norepinephrine. Certain smooth muscles are stimulated by these
neurotransmitters, whereas others are inhibited. A number of hormones also
influence the actions of smooth muscles. Smooth muscle contracts and relaxes
more slowly than skel-etal muscle. The whole muscular sheet responds to a
stimulus in unison because there is electrical cou-pling of smooth muscle cells
by gap junctions. This differs from
skeletal muscle, in which the fibers are electrically isolated from each other.
Skeletal muscle fibers are stimulated to contract by their own neu-romuscular
junctions. The gap junctions of smooth muscle allow the transmission of action
potentials from fiber to fiber. With the correct amount of ATP, it can maintain
forceful contractions for a longer period. Smooth muscles can change length
without changing how taut they are. A summary of smooth muscle contraction is
■■ The sliding filament mechanism occurs for the interaction of actin and
myosin.
■■ A rise in the intracellular calcium ion level is the final trigger for
contraction.
■■ ATP energizes the sliding process.
Smooth muscle takes approximately
30 times lon-ger than skeletal muscle to contract and relax. How-ever, it uses
much less energy. It can maintain the same amount of contractile tension for
long periods, with less than 1% of the energy expended. In small arterioles and
other visceral organs, the smooth mus-cle regularly maintains a small amount of
contraction (smooth muscle tone) with
fatigue. Because of its low energy requirements, the aerobic pathways of smooth
muscle manufacture adequate amounts of needed ATP.
Most adjacent smooth muscles have
slow, syn-chronized contractions, in which the whole muscu-lar sheet responds
in unison to stimuli. As discussed earlier, this is related to gap junctions,
which allow action potentials to be transmitted from fiber to fiber. The
pacemaker cells control the pace of contractions. The speed of the ATPases of
smooth muscle is much slower than in skeletal muscle. Myofilaments may con-nect
during prolonged contractions, which help save energy. The contraction of
smooth muscle is regulated by neural, hormonal, and local chemical factors.
■■ Neural regulation:
Neurotransmitter binding generates an
action potential. This is coupled to increased calcium ions in the cytosol.
Some types of smooth muscle only respond to neural stimulation with graded
potentials, which are local electrical signals. Different autonomic nerves
serve visceral smooth muscle, releasing different neurotransmitters. Each of
these can excite or inhibit groups of smooth muscle cells. This is based on the
type of receptor molecules on the sarcolemma of cells.
■■ Hormonal regulation: Hormones
are chemicals that have the ability
to affect smooth muscle con-traction. The hormone gastrin, for example,
sim-ulates the stomach to contract so that its churning actions of food are
more efficient.
■■ Local chemical regulation:
Smooth muscles that lack a nerve
supply depolarize sponta-neously or in response to chemicals that bind to
protein-linked receptors. Other smooth muscle cells may respond to chemical as
well as neural stimuli. Direct responses to chemical stimuli affects smooth
muscle activity based on local tissue needs. Chemical factors can cause
contraction or relaxation without action potentials by altering calcium ion
entry into the sarcoplasm. It is important to understand that chemical factors
may include some hormones as well as histamine, lack of oxygen, low pH, and
excess carbon dioxide.
Unique factors of smooth muscle
contraction include response to stretching and changes in length and tension.
Stretching of smooth muscle causes contraction, resulting in the automatic
movement of substances along internal tracts. The increased tension is only
brief and the smooth muscle quickly adapts to stretching, and then relaxes. It
is still able to contract as needed. Therefore, the stress relax-ation response
is important for organs such as the intestines and stomach, which must store
their con-tents for enough time so that digestion and nutrient absorption can
occur. The urinary bladder also must store urine, which is continuously made,
until it can be voided.
Smooth muscles vary in fiber
arrangement, fiber orga-nization, innervation, and how they respond to
stim-uli. There are two major types of smooth muscle:
■■ Visceral
smooth muscle: Also known as uni-tary smooth
muscle, it exists in the
walls of all hollow organs except for
the heart. It is the most common type of smooth muscle. Its cells are arranged
in opposing sheets, either circular or longitudinal. They are innervated by
auto-nomic nerve fiber varicosities. The cells often show rhythmic spontaneous action potentials. They are electrically
coupled by gap junctions. Therefore, the cells contract as a unit. Recruit-ment
is not utilized in unitary smooth muscle and it is able to respond to various
chemical stimuli. Visceral smooth muscle fibers can stim-ulate each other and
adjacent fibers experience excitability. They display a pattern of repeated contractions known as
rhythmicity, which is caused by
self-exciting fibers. The wave-like motion of many tubular organs, known as peristalsis, is caused by these features of vis-ceral smooth muscle.
Peristalsis helps to move the contents of organs such as the intestines from
the stomach to the outside of the body.
■■ Multiunit
smooth muscle: This type exists in the large lung airways, large arteries, arrector pili
muscles of the hair follicles, and the internal eye muscles that adjust the
pupils and allow the eyes to focus. Gap junctions and spontaneous depolarizations
are rare. Multiunit smooth mus-cle has fibers that are structurally independent
of each other. It has many nerve endings, with each forming a motor unit having
a number of mus-cle fibers. Multiunit smooth muscle, has only one nucleus,
responds to neural stimulation and has graded contractions involving
recruitment. It is also innervated by the autonomic nervous system and responds
to hormones.
1. Explain
the actions of pacesetter cells.
2. Discuss
the effects of gap junctions in smooth muscle.
3. Compare
visceral smooth muscle and multiunit smooth muscle.
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