Pedia News

Cardiac and Smooth Muscle

Cardiac and Smooth Muscle
Cardiac 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.
Cardiac And Smooth Muscle

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.