Muscle, contraction types

Muscle tissue is unique in its ability to shorten or contract. The human body has three basic types of muscle tissue histologically classified into smooth, striated, and cardiac muscle tissues. Only the striated muscle tissue is found in all skeletal muscles. The type of cells which compose the muscle tissue are known as contractile cells. They originate from mesenchymal cells which differentiate into myoblasts. Myoblasts are embryonic cells which later differentiate into contractile fiber cells. 

Dihydropyridine receptor (DHPR) is a member of voltage-dqiendent Ca2+ channels (CaVi, L-type), which specifically binds to dihydropyridine derivatives, a group of the Ca2+ channel blockers. Cav 1.1 works as the voltage sensor for skeletal muscle contraction, and Cay 1.2, as Ca2+-influx channel for cardiac muscle contraction. 

A large number of diugs interfere with the smooth muscle contraction. These compounds lower blood pressure and are referred to as antihypertensive. In this section, only those coumpounds will be mentioned that have a direct effect on smooth muscle tone. Phenylephrine is an agonist on most smooth muscles and activates ax adrenoceptors. Carbachol is an agonist on some smooth muscles and activates contraction through muscarinic receptors. Blockers of the ax-adrenoceptors such as prazosin and urapidil are competitive inhibitors of the ax-receptor in vascular and bladder smooth muscle. Phenoxybenzamine is an ineversible blocker of ax receptors and phentol-amine blocks ax and a2 receptors. Ca2+ channel blockers such as the dihydropyiidines, phenylalkyla-mines and benzothiazepines lower smooth muscle tone by blocking the L-type calcium channel. 

Although the fundamental chemomechanical transduction processes seem to be the same in all types of vertebrate muscle, contraction in smooth muscle is characterized by much greater involvement of enzymatically catalyzed control reactions. In smooth muscle the control reactions themselves involve the use of phosphorylation-dephosphorylation cycles. Moreover, they are futile in the sense they cause the expenditure of bond energy without a tangible work resultant, i.e., compounds synthesized or external work done. 

Hypothyroid myopathy occurs in about 30% of patients with hypothyroidism irrespective of its cause. Muscle pain, cramps, and stiffness may be seen, and are often exacerbated by cold weather. Pseudomyotonic features of delayed muscle contraction and relaxation are common. Myoedema (the mounding phenomenon) is due to the painless, electrically silent contracture produced on direct percussion. Muscle biopsy often shows a predominance of type 1 (slow-twitch) fibers, again analogous to that seen in experimental hypothyroidism (Figure 22). Muscle hypertrophy with weakness and slowness of movement occurs in the Debre-Semelaigne syndrome seen in severely hypothyroid children, and Hoffman s syndrome is a similar condition seen in adults with hypothyroidism, but is also accompanied by painful spasms. 

False negative muscle contraction tests are very rare. To date, a negative muscle contraction test rules out MH. A false negative test can be explained by the presence of two types of muscle fibers in a MH susceptible patient the response being dependent on the proportion of the two types of muscle fibers. The K-type designation is used to describe a patient who has a positive joint halothane-caffeine contracture, but a negative separate halothane or caffeine contracture. Whether K-type individuals are MH-susceptible or not is a controversial issue. 

Constipation can be due to primary and secondary causes (Table 18-1). Primary or idiopathic constipation is typified by normal-transit constipation, slow-transit constipation, and dyssynergic defecation. In the normal-transit type, colonic motility is unchanged and patients tend to experience hard stools despite normal movements. In the slow-transit type, motility is decreased leading to infrequent harder, drier stools. In dyssynergic defecation (also known as pelvic floor dysfunction), patients have lost the ability to relax the anal sphincter while coordinating muscle contractions of the pelvic floor. Some causes of secondary constipation are listed in Table 18-1. 

Tension-type headache (TTH) is the most common primary headache disorder. It is often underrepresented in clinical practice, as many patients do not present for care.6 The term tension-type headache is used to describe all headache syndromes in which muscle contraction is the most significant factor in the pathogenesis of pain. The 1-year prevalence of TTH in the population ranges from 30% to 90%.6 It is more common in adult females. Environmental factors, as opposed to genetic predisposition, play a more central role in their development. Tension-type headaches can be further divided into episodic or chronic the mean frequency of attacks is 3 days per month in episodic disorders, and chronic TTH is defined as 15 or more attacks in a 1-month period.7 The estimated prevalence of chronic TTH is less than 5%.6 Some researchers believe that chronic TTHs represent a continuum of headache severity with migraine headache.8 When severe headaches are difficult to differentiate clinically, treatment should initially target TTH. 

Dystonia A type of dyskinesia. The movement is slow and twisting. It may be associated with painful muscle contractions or spasms. 

Many activities require both types of muscle contraction. An example is running when one of the legs hits the ground, isometric contraction of the muscles within this limb keep it stiff and help to maintain body support. At the same time, isotonic contractions in the opposite leg move it forward to take the next stride. 

All types of muscle require calcium for contraction. In skeletal muscle, Ca++ ions are stored within an extensive membranous network referred to as the sarcoplasmic reticulum. This network is found throughout the muscle fiber and surrounds each myofibril. Furthermore, segments of the sarcoplasmic reticulum lie adjacent to each T tubule that, with a segment of sarcoplasmic reticulum on either side of it, is referred to as a triad. As the action potential is transmitted along the T tubule, it stimulates the release of Ca++ ions from the sarcoplasmic reticulum. The only source of calcium for skeletal muscle contraction is the sarcoplasmic reticulum. 

A pacemaker potential involves gradual depolarization of the cell membrane to threshold. The subsequent generation of an action potential causes smooth muscle contraction. This type of spontaneous depolarization is referred to as a "pacemaker potential" because it creates a regular rhythm of contraction. 

Increases in the concentration of calcium in the cytosol provides a signal that can initiate muscle contraction, vision, and other signaling pathways. The response depends on the cell type. In muscle, a transient rise in the cytosolic calcium levels (from opening calcium channels in the sarcoplasmic reticulum) causes contraction. This signaling in contraction is a direct consequence of electrical activation of the voltage-gated channel. 

An initial hint that Ca2+ stores are present and functional in smooth muscle cells came from earlier experiments revealing that agonist-induced contractions could be observed in the absence of extracellular Ca2+. It is now known that smooth muscle Ca2+ stores express two types of Ca2+ release channels, the ryanodine receptor (RyR) and the inositol-1,4,5-trisphosphate (L1SP3) receptor (L1SP3R) (Somlyo Somlyo 1994). Recent studies have shown that Ca2+ release from intracellular Ca2+ stores plays various important roles in the regulation of smooth muscle contraction. Local and transient releases of Ca2+ from RyR near the surface membrane, which are called Ca2+ sparks, activate Ca2+-sensitive K+... 

Ca2+ is the major second messenger in the activation of smooth muscle contraction. Thus smooth muscle Ca2+ handling is of major importance to understanding its function. Ca2+ homeostasis is a balance of Ca2+ influx and extrusion. Influx is generally through channels, such as I, or T type Ca2+ channels or the so-called capacitive entry pathway, through stretch activated channels, leak pathways and reversed mode Na+/Ca2+ exchanger, which may... 

In contrast, skeletal muscle contraction is more rapid than that of smooth muscle but skeletal muscle cannot maintain the same tone for long periods of time. As indicated in Table 7.1, we can distinguish sub-types of muscle fibre within... 

In addition to the displacement of caldesmon, smooth muscle cell contraction requires kinase-induced phosphorylation of myosin. Smooth muscle has a unique type of myosin filament called p-light chains which are the target (substrate) for MLCK, but MLCK is only active when complexed with CaCM. Myosin light chain phosphatase reverses the PKA-mediated process and when cytosolic calcium ion concentration falls, CDM is released from CaCM and re-associates with the actin. The central role of calcium-calmodulin in smooth muscle contraction is shown in Figure 7.4. 

In addition to energy reserves, many other types of biochemicals are required to maintain an organism. Cholesterol is required for cell membrane structure, proteins for muscle contraction, and polysaccharides for the intracellular matrix, to name just a few examples. These substances may be produced from transformed dietary components. 

Okadaic acid is a powerful tumor promoter of a nonphorbol ester type that inhibits protein phosphatase-1 and -2A in vitro (Haystead et al., 1989). Okadaic acid directly stimulates smooth muscle contraction (Haystead et al., 1989) and probably causes diarrhea, either by stimulating the phosphorylation of proteins controlling sodium secretion by intestinal cells or by increasing phosphorylation of elements that regulate permeability to solutes, resulting in a passive loss of fluids (Aune and Yndestad, 1993). 

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