Cardiac and Smooth Muscle.
The muscles of the heart, the myocardium,
generate the force of contraction of the atrial and ventricular muscles. The
myocardium is composed of cardiac muscle cells called myocytes. These
cells are striated due to the orderly arrangement of the thick and thin
filaments which, as in skeletal muscle, make up the bulk of the muscle.
However, they are less organized than in skeletal muscle (Fig. 15a,b). The myocytes
have dimensions of 100 × 20 μm, are branched, with a single nucleus,
and are also rich in mitochondria. The normal pumping action of the
heart is dependent on the synchronized contraction of all cardiac cells. Their
contraction is not dependent on an external nerve supply, as in skeletal
muscle, but instead the heart generates its own rhythm, called inherent
rhythmicity. The nerves innervating the heart only speed up or slow down
the rhythm and can modify the force of contraction (the so-called chronotropic
and inotropic effects respectively; Chapter 19).
The synchronicity between myocytes
occurs because all the adjacent cells are linked to one another at their ends
by specialized gap or electrotonic junctions – intercalated
discs – which are essentially low-resistance pathways between cells. These
allow action potentials to spread rapidly from one cell to another and enable
the cardiac muscle to act as a functional syncytium (i.e. it acts as a
single unit although comprising individual cells).
The intercalated discs provide both
a structural attachment (desmosomes) between cells and an electrical
contact, called a gap junction, made up of proteins called connexons (Fig.
15a). Although a rise in intracellular Ca2+ initiates contraction in
the same way as in skeletal muscle (Chapter 12), the mechanisms leading to this
rise in intracellular Ca2+ are fundamentally different, and are
discussed in Chapter 19.
Smooth muscle
The absence of striations within
the cells and the poorer organization of the fibres give this type of muscle
its name. Each cell contains only one nucleus situated near the centre.
Smooth muscle is involved in many involuntary processes in blood vessels and
the gut.
The smooth muscle of each organ is
distinctive from that of most other organs, and there is considerable variation
in the structure and function of smooth muscle in different parts of the body;
however, essentially it can be divided into unitary (or visceral)
and multiunit smooth muscle types.
Smooth muscle cells are
spindle-shaped with dimensions of 50–400 μm in length by 2–10 μm thick. They
are joined, like cardiac muscle, by special intercellular connections called desmosomes.
Because the actin and myosin filaments are not regularly arranged, they lack
striations. Smooth muscle cells shorten by sliding of the myofilaments towards
and over one another, but at a much slower rate than in other muscle types. For
this reason, they are capable of pro- longed, maintained contraction, without
fatigue and with little energy consumption (Fig. 15c).
The unitary muscle type or visceral
smooth muscle exhibits many gap junctions between cells, and a steady wave
of contraction can pass through a whole sheet of muscle as if it were a single
unit. It is commonly found in the stomach, intestines, urinary bladder, urethra
and blood vessels, and is capable
of bringing about autorhythmical activity (seen particularly in the
digestive tract where it is modulated by neuronal activity).
Tonic activity causes smooth muscle to remain in a constant
state of contraction or tonus. It is commonly found in sphincters that control
the movement of digestive products through the gastrointestinal tract. Multiunit
smooth muscle is made up of individual fibres not connected by gap
junctions, but separately stimulated by autonomic motor neurones. Each smooth
muscle fibre can contract independently from the others. Examples include the
ciliary muscles of the eye, the iris of the eye and piloerector muscles that
cause erection of hairs when stimulated
by the sympathetic system.
The factors that influence the
neural control of smooth muscle are:
1 The type
of innervation and the transmitter released.
2 The
receptor of the neurotransmitter on the muscle cell itself.
3 The
anatomical arrangement of the nerve in relation to the muscle fibres.
There are three types of
innervation: extrinsic – from the autonomic part of the nervous system,
mainly sympathetic (arteries), parasympathetic (ciliary muscles) and both
sympathetic and parasympathetic (gut); intrinsic – a plexus of nerves
within the smooth muscle itself (seen in the gut); and afferent sensory
neurones – these indirectly lead to the reflex activation of motor
neurones.
Smooth muscle cells also respond to
local tissue factors and hormones, i.e. changes in the fluids that surround
them (interstitial fluids). In addition, many hormones that circulate in the
bloodstream also cause smooth muscle contraction [hormones such as adrenaline
(epinephrine), angiotensin, oxytocin, antidiuretic hormone (ADH), noradrenaline
(norepinephrine) and serotonin]. Also, a lack of oxygen in the tissues causes
smooth muscle cells to relax and vasodilate; an increase in CO2 or H+ also causes vasodilatation
(Chapter 21).
Contractile mechanisms
of smooth muscle Smooth muscle contains no troponin, but has twice as much actin and
tropomyosin as striated muscle. Myosin is also present, but only in about
one-quarter of the amount found in striated muscle fibres. The rate at which
cross-bridges are formed and released is slower (some 300 times) than that in
striated muscle fibres, in part due to the different mechanisms involved.
Although contraction of smooth
muscle is initiated by an increase in Ca2+, unlike striated muscle
this is not mediated via the interaction of Ca2+ with troponin
(there is none). Instead, cross-bridge formation is controlled from the myosin
side in a rather more complex fashion. Ca2+ binds to the protein calmodulin,
which activates myosin light chain kinase. This phosphorylates myosin
which allows it to form cross-bridges with actin, using energy from adenosine
triphosphate (ATP). It follows that there must be a means by which myosin is
dephosphorylated. This is provided by myosin phosphatase. Many factors
that contract smooth muscle do so by inhibiting myosin phosphatase at the
same time as raising Ca2+, so maximising the degree of myosin
phosphorylation (Chapter 21). A comparison of the properties of
skeletal, cardiac and smooth muscle
is shown in the Appendix I.
