Трифонов Е.В.
Антропология:   дух - душа - тело - среда человека,

или  Пневмапсихосоматология человека

Русско-англо-русская энциклопедия, 18-е изд., 2015

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Общий предметный алфавитный указатель

Психология Соматология Математика Физика Химия Наука            Общая   лексика
А Б В Г Д Е Ж З И К Л М Н О П Р С Т У Ф Х Ц Ч Ш Щ Э Ю Я
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z


ГЛАДКАЯ МЫШЦА
smooth muscle ]

     Гладкая мышца - орган тела человека (животных), основой структуры которого является гладкая мышечная ткань.
     Нередко термин «мышца» используется как синоним термина «мышечная ткань». Например, говорят «поперечнополосатая мышца», «гладкая мышца», имея в виду поперечнополосатую мышечную ткань, гладкую мышечную ткань. При использовании этих синонимов следует учитывать, что поперечнополосатая мышечная ткань действительно чаще всего образует органы: скелетные мышцы и сердце - мышечный орган. Гладкая мышечная ткань самостоятельные органы - мышцы, состоящие в основном из гладкой мышечной ткани, образует значительно реже. Чаще она остается тканью, образующей слои, оболочки в составе всех внутренних органов. В последнем случае более определенным следует считать употребление термина «мышечная ткань», но не «мышца». Например, гладкой мышечной тканью образованы мышечные оболочки кровеносных и лимфатических сосудов, мышечные оболочки дыхательных путей, мышечная оболочка нижней трети пищевода, трехслойная мышечная оболочка желудка, мышечные оболочки кишок, трехслойная мышечная оболочка семявыносящего протока, трехслойная мышечная оболочка мочевого пузыря, трехслойная мышечная оболочка мочеточника, трехслойная мышечная оболочка матки и т.д.
     Примеры гладких мышц: ресничная мышца, участвующая в аккомодации глаза, мышца, расширяющая зрачок, мышца, суживающая зрачок и т.д.

Схема. Структура типичного лейомиоцита.
Модификация: Berridge, M.J. Cell Signalling Biology, 2012., см.: http://www.biochemj.org/csb/frame.htm.

Обозначения:

Structure of a typical smooth muscle cell. One end of the actin filament is tethered to a dense body, which is either attached to the plasma membrane or lies free within the cytoplasm. The dense bodies, which provide the anchorage points between the contractile filaments and the plasma membrane, contain ?-actinin and vinculin and appear to be analogous to the Z lines in skeletal muscle.


Smooth muscle cells = http://www.biochemj.org/csb/frame.htm Smooth muscle cells are a heterogeneous collection of cell types that function in many different organs, where they regulate a variety of functions such as vascular smooth muscle control of blood vessel tone, emptying of the bladder, tonic contractions of sphincters such as the urethra and the rhythmical contraction of the gastrointestinal tract, uterus and ureter. In order to carry out these multiple functions, a number of different signalling mechanisms have evolved to control smooth muscle contractility. There is a certain degree of uniformity with regard to smooth muscle cell structure and there also are some general mechanisms that are responsible for smooth muscle cell excitation–contraction coupling . In addition to this excitatory mechanism, there also are signalling pathways responsible for smooth muscle cell relaxation . However, when it comes to the smooth muscle activation mechanisms , each muscle has to be considered separately especially with regard to the way in which excitatory stimuli bring about the increase in Ca2+ necessary to trigger contraction. Most smooth muscle cells are excited by membrane depolarization that then activates VOCs to provide the Ca2+ signal to induce contraction. For many of these muscles, this depolarization is induced by the interstitial cells of Cajal that have a pacemaker function resembling that of the sino-atrial node in the heart. Other smooth muscles have an endogenous pacemaker mechanism while others are activated directly by neurotransmitters released by nerves. Smooth muscle cell structure Smooth muscle cells have a spindle shape, and are usually lined up alongside each other and are connected through gap junctions (Module 7: Figure smooth muscle cell structure ). They are about 100 ?m long and 5–10 ?m wide. The cell surface has numerous caveolae and many of these make close contact with the sarcoplasmic reticulum (Module 6: Figure smooth muscle caveolae). By comparison with skeletal and cardiac muscle, the contractile system composed of actin and myosin is somewhat disorganized, with actin filaments radiating away from localized densities dotted around the plasma membrane. Smooth muscle cell contraction also differs from that found in skeletal and cardiac muscle in that there are two different mechanisms for regulating the contractile processes (Module 7: Figure smooth muscle cell E-C coupling ): Smooth muscle cell excitation–contraction coupling Excitation–contraction coupling refers to the mechanism whereby the smooth muscle cell contracts in response to excitatory stimuli. Most smooth muscle activation mechanisms result in depolarization of the membrane that then initiates the smooth muscle Ca2+ signalling cascades that lead to contraction. In addition, there is a smooth muscle Rho/Rho kinase signalling pathway that bring about contraction. Uterine smooth muscle cells The uterus is made up of three parts: the body that makes up the major part, a domed-shape fundus at the top and the cervix at the bottom (Module 7: Figure urinogenital tract ). Most of the uterus is composed of the myometrium, which is a thick layer of longitudinal and circular smooth muscle cells. Within each layer, the smooth muscle cells are arranged in individual bundles (fasciculus) that lie parallel to each other and are connected through gap junctions. During early pregnancy, the uterus is relatively quiescent. There are a few weak twitches resulting from unsynchronized smooth muscle cell contractions. With the onset of labour, the uterus begins to develop stronger and more frequent contractions that appear first in the fundus and then spread rapidly through the body of the uterus. This remarkable switch from quiescence to a cycle of strong contractions is an example of the phenotypic remodelling of the signalsome, which in this case is the endogenous uterine smooth muscle activation mechanism. For example, there is an increase in gap junctional coupling just before labour. There is an increase in the expression of PDE4B, which decreases the effect of tocolytic agents such as ?-adrenergic agents that use cyclic AMP to inhibit uterine contractions. There is an increase in the expression of the oxytocin receptors that act by inducing and accelerating contractions. The expression of the ryanodine receptor 2 (RYR2) is up-regulated during pregnancy and this may facilitate the process of excitation–contraction coupling. A decline in the activity of the Na+-K+-ATPase pump during labour may accelerate the uterus smooth muscle cell membrane oscillator and thus contribute to the increase in the frequency of contractions. There may also be a decrease in the activity of potassium channels such as TREK-1 and the large-conductance (BK) channels that contributes to the quiescence of the uterus during pregnancy. The next aspect to consider is how this remodelled signalsome switches the uterus out of its quiescent state such that it begins to generate the repetitive electrical impulses responsible for driving contractions during labour. The uterine contractions that occur during labour have a periodicity of approximately 3–5 min (see Module 7: human uterine contractions and Module 7: Figure Ni2+ slows uterine oscillations ). They have a characteristic shape; there is a slow rising phase (15 s), a plateau that lasts for about 30 s that is followed by a gradual relaxation phase that is roughly symmetrical with the rising phase. Each of these protracted uterine contractions depends upon the co-ordinated activation of most of the smooth muscle cells and this synchronicity is achieved by an action potential spreading through the smooth muscle cell layer with a conduction velocity of approximately 4 cm/s. The wave of excitation appears to begin at the fundus and then spreads through the body of the uterus towards the cervix. Even though all smooth muscle cells in the uterus are capable of generating a rhythm, those in the fundus are inherently more rhythmical and thus initiate each contraction wave. Since there appear to be no interstitial cells of Cajal and there is little neural innervation, the uterine myometrium is driven by an endogenous pacemaker mechanism (see A in Module 7: Figure SMC activation mechanisms ). Some of the features of this pacemaker mechanism are illustrated in Module 7: human uterine contractions . The regular rhythm is accelerated reversibly by oxytocin. Perhaps the most interesting feature of the rhythm is that it continues and is accelerated by the drug cyclopiazonic acid (CPA) that blocks the sarco/endo-plasmic reticulum Ca2+-ATPase (SERCA) pump and thus empties the internal store of Ca2+. This observation rules out the presence of a cytosolic oscillator and suggests that the pacemaker is driven by a membrane oscillator. The activation mechanism thus has two main components (Module 7: Figure uterus activation ). A membrane oscillator (horizontal box), which generates a pacemaker depolarization (?V), and L-type VOCs that respond to depolarization with a fairly typical smooth muscle cell excitation–contraction coupling mechanism (vertical green box). The primary signal for triggering contraction is the Ca2+ that enters the cell through the L-type VOC. There appears to be little role for release of Ca2+ from the internal stores since contractions continue when these stores have been depleted. However, there is an increased expression of RYR2s during the end of pregnancy and these may open in response to the entry of external Ca2+ to provide an additional boost of Ca2+ to increase the force of contraction (Module 7: Figure uterus activation ). However, the major activation mechanism for contraction is the opening of the L-type channels by the membrane depolarization provided by the action potential that sweeps through the uterine smooth muscle cell syncytium. While the nature of the excitation–contraction coupling mechanism is fairly well established, there is less information on the nature of the uterus smooth muscle cell membrane oscillator that is responsible for generating the periodic action potentials. Uterus smooth muscle cell membrane oscillator The nature of the pacemaker mechanism responsible for generating the action potentials that drive the smooth muscle contraction cycles during labour is still a mystery. The following membrane oscillator model attempts to explain the mechanism responsible for the slow pacemaker depolarization that triggers each contraction and how the frequency of this oscillator is modulated by stimuli such as oxytocin (Module 7: Figure uterus activation ). The shape of the membrane potential fluctuation that drives each contractile cycle has two main components: there is a slow pacemaker depolarization that brings the membrane potential to the threshold (dashed line in Module 7: Figure uterus activation ) for the action potential that is driven by the opening of the L-type VOCs. At the end of the action potential, the membrane potential switches back to a hyperpolarized state before beginning the next pacemaker depolarization phase. The critical question with regard to uterine contractility is the nature of the membrane oscillator that drives this slow pacemaker depolarization. At any moment in time, membrane potential depends upon the co-ordinated activity of ion channels, pumps and exchangers that can either depolarize or hyperpolarize the membrane. At the end of the action potential, the hyperpolarizing components are dominant but as their influence wanes the depolarizing components begin to take over to produce the pacemaker depolarization. There are a number of candidates that could contribute to this hyperpolarizing/depolarizing switch (see the membrane oscillator box in Module 7: Figure uterus activation where the components that contribute to depolarization or hyperpolarization are coloured green and red respectively). At present, it is not clear how or when these possible contenders might contribute to the membrane oscillator during the course of the pacemaker depolarization. These different candidates have been included in the model based on either physiological evidence or the fact that they are expressed in human uterine or other smooth muscle cells as outlined below (Module 7: Figure uterus activation ). K+ channels A number of K+ channels regulate uterine contraction. Both the large-conductance (BK) channels and the small-conductance (SK) channels are expressed in uterine smooth muscle and may contribute to the membrane oscillator. Activation of the BK and SK3 channels by Ca2+ contribute to the repolarizing phase of the action potential and may thus determine the maximal hyperpolarizing potential at the start of the pacemaker phase. As Ca2+ is pumped out of the cell, their hyperpolarizing influence will wane and this will contribute to the gradual pacemaker depolarization. Inhibition of the SK3 channel with apamin results in an acceleration of the oscillator. Conversely, if SK3 is overexpressed in rat uterus, there is a drastic reduction in oscillator frequency. In addition to contributing to the membrane oscillator during labour, the BK channel may also play a role in maintaining the quiescent state of the uterus during pregnancy. These BK channels appear to be concentrated in the numerous caveolae that are a characteristic feature of smooth muscle cells (Module 7: Figure smooth muscle cell structure ). These infoldings of the surface membrane, which often come into close contact with the endoplasmic reticulum (ER) (Module 6: Figure smooth muscle caveolae), have numerous signalling components and are rich in lipids such as cholesterol and sphingomyelin (SM) (Module 6: Figure caveolae organization). The cholesterol appears to function by enhancing the activity of the BK channels to reduce membrane excitability and thus contribute to the quiescent state. The increases in cholesterol that accompany obesity may increase the risk of complications in pregnancy by reducing the uterine contractility during labour and may account for the increased incidence of Caesarean sections in obese women. The normal uterus contracts when stretched, but this excitability is reduced during pregnancy through the expression of stretch-sensitive TREK-1 channels and this enanles the uterus to distend. At the end of pregnancy, a decrease in TREK-1 expression enhances excitability and thus contributes to the onset of labour. Na+-K+-ATPase pump During the course of the action potential, opening of the L-type VOC results in Na+ entering the cell together with Ca2+. A hyperpolarization is generated when the Na+ is removed by the Na+ pump, which is electrogenic because it extrudes 2Na+ for 3K+. The pump will be activated immediately after an action potential to extrude Na+ and this will contribute to the early hyperpolarizing phase. But as the Na+ concentration returns to resting levels, this hyperpolarizing effect will decline and this may contribute to the depolarizing pacemaker. Na+/Ca2+-exchanger (NCX) The Na+/Ca2+-exchanger (NCX) has a somewhat ambiguous role because it can operate in both a forward and reverse mode (Module 5: Figure Na+/Ca2+-exchangers) and thus can contribute to either depolarization or hyperpolarization. The resting membrane potential of the uterus as it begins to oscillate is approximately -50 mV, which is probably more positive than the equilibrium potential for Na+, so it is likely that the exchanger will be operating in its reverse mode as shown in Module 7: Figure uterus activation . When operating in its reverse mode, 1Ca2+ is exchanged for 3Na+ so this stoichiometry may also favour hyperpolarization. Store-operated Ca2+ channel (SOC) Smooth muscle cells are known to express store-operated channels (SOCs) and these have been included as one of the possible channels for providing the inward current that is necessary to provide the depolarizing drive during the pacemaker depolarization. In addition, such a SOC mechanism may help to describe how oxytocin can accelerate the membrane oscillator. The suggestion is that oxytocin stimulates the formation of InsP3 that then acts to empty part of the endoplasmic reticulum (ER) store that lies near the membrane to promote the opening of the SOC and this increase in inward current will steepen the pacemaker depolarization to accelerate the oscillator. Another possibility is that the Ca2+ that enters the cell may act to switch on channels such as the Ca2+-sensitive chloride channels (CLCA). Ca2+ may also activate TRPM4 or TRPM5 that gate an inward monovalent current and have been implicated in the operation of other membrane oscillators. CaV3 T-type channels Uterine smooth muscle cells express CaV3.1, which is one of the isoforms of the CaV3.1 family of T-type channels (Module 3: Table VOC classification), which have been implicated in the pacemaker activity of other excitable cells. At the low membrane potential of activated uterine smooth muscle cells, these T-type channels are probably inactivated. However, at these inactivation potentials, a small population may still contribute to a pacemaker depolarization by gating an inward flux of Ca2+. Such a role for the T-type channel is consistent with the observation that low concentrations of Ni2+ slow the oscillator (Module 7: Figure Ni2+ slows uterine oscillations ). The entry of Ca2+ through these T-type channels may also contribute to the depolarization by activating other inward currents such as those gated by TRPM4 or TRPM5 as mentioned above. Ca2+-sensitive chloride channels A proportion of human uterine cells express Ca2+-sensitive chloride channels (CLCA), which could play an important role in providing the inward current to drive pacemaker depolarization (Module 7: Figure uterus activation ). TRPM4 and TRPM5 TRPM4 and TRPM5, which are members of the melastatin-related transient receptor potential (TRPM) family of ion channels, respond to an increase in Ca2+ by gating an inward current carried by monovalent cations such as Na+. Although there is no information yet on their expression in uterine smooth muscle, they are known to occur in other smooth muscle cell types. These channels are not shown in Module 7: Figure uterus activation , but they should also be considered in the model because they could play a critical role in the pacemaker mechanism by providing an inward current to drive the pacemaker depolarization. Hyperpolarizing-activated cyclic nucleotide-gated (HCN) channels A number of cells that display pacemaker activity express members of the hyperpolarizing-activated cyclic nucleotide-gated (HCN) channels, which have been described in rat uterine smooth muscle. They have been included in the model (Module 7: Figure uterus activation ) because they are one of the major pacemaker channel currents in the sinoatrial (SA) node pacemaker cells that has a similar membrane oscillator (Module 7: Figure cardiac pacemaker ). In conclusion, uterine contraction is driven by a membrane oscillator that consists of multiple components that can either depolarize or hyperpolarize the membrane. At the end of the action potential, the hyperpolarizing elements predominate but as these wane and the depolarizing components begin to take over the membrane gradually depolarizes to the point where the next action potential and contraction are triggered. Many of the hormones that modulate contractility are likely to influence some of these oscillatory components. For example, it is argued that oxytocin may act to switch on a SOC to provide an inward Ca2+ current that not only contributes a depolarizing signal but it also may act to switch on some of the TRPM channels. Oxytocin may have additional actions because it can increase the force of contraction in muscle cells where the internal stores have been depleted of Ca2+ following treatment with CPA (Module 7: human uterine contractions ). In this case, it seems likely that oxytocin may switch on the smooth muscle Rho/Rho kinase signalling pathway to enhance the sensitivity of the contractile mechanism. It is difficult to speculate further on how contractility is modulated until the nature of the membrane oscillator has been established. This is an important priority because problems remain concerning an effective treatment of controlling premature labour, which is one of the major causes of neonatal morbidity.

Схема. Механизм сопряжения возбуждение-сокращение лейомиоцита.
Модификация: Berridge, M.J. Cell Signalling Biology, 2012., см.: http://www.biochemj.org/csb/frame.htm.

Обозначения:

Smooth muscle cell excitation–contraction (E-C) coupling mechanisms. A network of signalling pathways is responsible for smooth muscle excitation–contraction (E-C) coupling. Ca2+ is derived from three sources: it can enter the cell through L-type voltage-operated channels (VOCs), it can be released by ryanodine receptors (RYRs) from internal stores or it can be released by inositol 1,4,5-trisphosphate (IP3). Ca2+ acts through calmodulin (CaM) to stimulate a myosin light chain kinase (MLCK), which phosphorylates the regulatory myosin light chain (MLC) to enable the myosin heads to interact with actin to initiate the contraction cycles. Sensitization of the Ca2+ signalling system is carried out through a Rho/Rho kinase signalling pathway that phosphorylates a myosin phosphatase targeting subunit 1 (MYPT1), which then inactivates the catalytic protein phosphatase 1 (PP1) to prevent it from dephosphorylating the regulatory light chains.

Схема. Циклический гуанозинмонофосфат/оксид азота как средства управления расслаблением лейомиоцита.
Модификация: Berridge, M.J. Cell Signalling Biology, 2012., см.: http://www.biochemj.org/csb/frame.htm.

Обозначения:

Function of the nitric oxide (NO)/cyclic GMP signalling pathways in controlling relaxation of smooth muscle cells. Nitric oxide (NO) acts on the soluble guanylyl cyclase (sGC) to form cyclic GMP (cGMP), which acts through a number of targets to dampen both the Ca2+ - and Rho-dependent signalling mechanisms that induce contraction by increasing the phosphorylation of the myosin light chain attached to the myosin.

Схема. Роль ионов кальция в управлениии сокращением/расслаблением лейомиоцита.
Модификация: Berridge, M.J. Cell Signalling Biology, 2012., см.: http://www.biochemj.org/csb/frame.htm.

Обозначения:

Function of smooth muscle cell Ca2+ sparks in the regulation of membrane potential and contraction/relaxation. Local and global Ca2+ signalling in smooth muscle cells can determine whether the muscle contracts or relaxes, as described in the text.

Схема. Механизмы активации лейомиоцитов ионами кальция.
Модификация: Berridge, M.J. Cell Signalling Biology, 2012., см.: http://www.biochemj.org/csb/frame.htm.

Обозначения:

Smooth muscle cell Ca2+ activation mechanisms. There are three main mechanisms responsible for generating the Ca2+ transients that trigger contraction. See text for further details.


     Литература.  Иллюстрации.     References.  Illustrations
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  1. Berridge M.J. Cell Signalling Biology, BJ Signal, 2012.
    Учебное пособие. Сайт.  Перевести на русский язык = Translate into Russian.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.biochemj.org/csb/default.htm          quotation
  2. Garfield R.E., Somlyo A.P., Grover A.K., Daniel E.E., Eds. Calcium and Contractility: Smooth Muscle = Кальций и сократимость гладкой мышцы. Humana Press, 1985, 497 p.
    Учебное пособие.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0          quotation
  3. Kao C.Y., Carsten M.E., Eds. Cellular Aspects of Smooth Muscle Function = Функции гладкой мышцы. Клеточные аспекты. Cambridge University Press, 2005, 312 p.
    Учебное пособие.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0          quotation
  4. Coburn R.F., Ed. Airway smooth muscle in health and disease = Гладкие мышцы дыхательных путей у здоровых и больных. Plenum Press, 1989, 324 p.
    Учебное пособие.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0          quotation
  5. Moreland R.S., Ed. Regulation of Smooth Muscle Contraction = Регуляция сокращения гладкой мышцы. Plenum Press, 1991, 546 p.
    Учебное пособие.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0          quotation
  6. Murthy K.S. Signaling for Contraction and Relaxation in Smooth Muscle of the Gut = Сигналы для сокращения и расслабления гладких мышц желудочно-кишечного тракта. Annual Review of Physiology, 2006, 68, 1, 345-374. Обзор.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0          quotation
  7. Sanders K.M. Regulation of smooth muscle excitation and contraction = Регуляция гладкомышечного сокращения и расслабления. Neurogastroenterology & Motility, 2008, 20, s1, 39-53. Обзор.
    Доступ к данному источнику = Access to the reference.
    URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0          quotation


См.: Миология: Словарь,
         Миология: Литература. Иллюстрации,

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    Т Е С Т    В А Ш Е Г О    И Н Т Е Л Л Е К Т А

Предпосылка:
Эффективность развития любой отрасли знаний определяется степенью соответствия методологии познания - познаваемой сущности.
Реальность:
Живые структуры от биохимического и субклеточного уровня, до целого организма являются вероятностными структурами. Функции вероятностных структур являются вероятностными функциями.
Необходимое условие:
Эффективное исследование вероятностных структур и функций должно основываться на вероятностной методологии (Трифонов Е.В., 1978,..., ..., 2015, …).
Критерий: Степень развития морфологии, физиологии, психологии человека и медицины, объём индивидуальных и социальных знаний в этих областях определяется степенью использования вероятностной методологии.
Актуальные знания: В соответствии с предпосылкой, реальностью, необходимым условием и критерием... ...
о ц е н и т е   с а м о с т о я т е л ь н о:
—  с т е п е н ь  р а з в и т и я   с о в р е м е н н о й   н а у к и,
—  о б ъ е м   В а ш и х   з н а н и й   и
—  В а ш   и н т е л л е к т !


Любые реальности, как физические, так и психические, являются по своей сущности вероятностными.  Формулирование этого фундаментального положения – одно из главных достижений науки 20-го века.  Инструментом эффективного познания вероятностных сущностей и явлений служит вероятностная методология (Трифонов Е.В., 1978,..., ..., 2014, …).  Использование вероятностной методологии позволило открыть и сформулировать важнейший для психофизиологии принцип: генеральной стратегией управления всеми психофизическими структурами и функциями является прогнозирование (Трифонов Е.В., 1978,..., ..., 2012, …).  Непризнание этих фактов по незнанию – заблуждение и признак научной некомпетентности.  Сознательное отвержение или замалчивание этих фактов – признак недобросовестности и откровенная ложь.


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Санкт-Петербург, Россия, 1996-2015

Copyright © 1996-, Трифонов Е.В.

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