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Advances in Physiology Education Dec 2003This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those... (Review)
Review
This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those professionals who are in need of an update on smooth muscle physiology may find this review to be useful. Smooth muscle lacks the striations characteristic of cardiac and skeletal muscle. Layers of smooth muscle cells line the walls of various organs and tubes in the body, and the contractile function of smooth muscle is not under voluntary control. Contractile activity in smooth muscle is initiated by a Ca(2+)-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca(2+) sensitization of the contractile proteins is signaled by the RhoA/Rho kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase, thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of myosin phosphatase initiate the process of smooth muscle relaxation.
Topics: Calcium; Humans; Muscle Contraction; Muscle Relaxation; Muscle, Smooth
PubMed: 14627618
DOI: 10.1152/advan.00025.2003 -
Physiological Reviews Jul 2004The detrusor smooth muscle is the main muscle component of the urinary bladder wall. Its ability to contract over a large length interval and to relax determines the... (Review)
Review
The detrusor smooth muscle is the main muscle component of the urinary bladder wall. Its ability to contract over a large length interval and to relax determines the bladder function during filling and micturition. These processes are regulated by several external nervous and hormonal control systems, and the detrusor contains multiple receptors and signaling pathways. Functional changes of the detrusor can be found in several clinically important conditions, e.g., lower urinary tract symptoms (LUTS) and bladder outlet obstruction. The aim of this review is to summarize and synthesize basic information and recent advances in the understanding of the properties of the detrusor smooth muscle, its contractile system, cellular signaling, membrane properties, and cellular receptors. Alterations in these systems in pathological conditions of the bladder wall are described, and some areas for future research are suggested.
Topics: Animals; Hormones; Humans; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Nervous System; Nervous System Physiological Phenomena; Urinary Bladder; Urinary Bladder Diseases; Urinary Bladder Neck Obstruction; Urologic Diseases
PubMed: 15269341
DOI: 10.1152/physrev.00038.2003 -
Cell Calcium May 2017Contraction is a central feature for skeletal, cardiac and smooth muscle; this unique feature is largely dependent on calcium (Ca) signaling and therefore maintenance of... (Review)
Review
Contraction is a central feature for skeletal, cardiac and smooth muscle; this unique feature is largely dependent on calcium (Ca) signaling and therefore maintenance of internal Ca stores. Stromal interaction molecule 1 (STIM1) is a single-pass transmembrane protein that functions as a Ca sensor for the activation store-operated calcium channels (SOCCs) on the plasma membrane in response to depleted internal sarco(endo)plasmic (S/ER) reticulum Ca stores. STIM1 was initially characterized in non-excitable cells; however, evidence from both animal models and human mutations suggests a role for STIM1 in modulating Ca homeostasis in excitable tissues as well. STIM1-dependent SOCE is particularly important in tissues undergoing sustained contraction, leading us to believe STIM1 may play a role in smooth muscle contraction. To date, the role of STIM1 in smooth muscle is unknown. In this review, we provide a brief overview of the role of STIM1-dependent SOCE in striated muscle and build off that knowledge to investigate whether STIM1 contributes to smooth muscle contractility. We conclude by discussing the translational implications of targeting STIM1 in the treatment of smooth muscle disorders.
Topics: Animals; Calcium Channels; Humans; Muscle Contraction; Muscle, Smooth; Stromal Interaction Molecule 1
PubMed: 28372809
DOI: 10.1016/j.ceca.2017.02.007 -
Archives of Biochemistry and Biophysics Mar 2019Mitochondria are important for airway smooth muscle physiology due to their diverse yet interconnected roles in calcium handling, redox regulation, and cellular... (Review)
Review
Mitochondria are important for airway smooth muscle physiology due to their diverse yet interconnected roles in calcium handling, redox regulation, and cellular bioenergetics. Increasing evidence indicates that mitochondria dysfunction is intimately associated with airway diseases such as asthma, IPF and COPD. In these pathological conditions, increased mitochondrial ROS, altered bioenergetics profiles, and calcium mishandling contribute collectively to changes in cellular signaling, gene expression, and ultimately changes in airway smooth muscle contractile/proliferative properties. Therefore, understanding the basic features of airway smooth muscle mitochondria and their functional contribution to airway biology and pathology are key to developing novel therapeutics for airway diseases. This review summarizes the recent findings of airway smooth muscle mitochondria focusing on calcium homeostasis and redox regulation, two key determinants of physiological and pathological functions of airway smooth muscle.
Topics: Animals; Bronchi; Calcium; Homeostasis; Humans; Lung Diseases; Mitochondria, Muscle; Muscle, Smooth
PubMed: 30629957
DOI: 10.1016/j.abb.2019.01.002 -
Basic & Clinical Pharmacology &... Jan 2012Blood vessel structure and calibre are not static. Rather, vessels remodel continuously in response to their biomechanical environment. Vascular calibre is dictated by... (Review)
Review
Blood vessel structure and calibre are not static. Rather, vessels remodel continuously in response to their biomechanical environment. Vascular calibre is dictated by the amount, composition and organization of the elastic extracellular matrix. In addition, the amount and organization of contractile smooth muscle cell (SMC) also need to be regulated. The SMCs are organized such that maximum contractile force generally occurs at diameters slightly below the diameter at full dilation and physiological pressure. Thus, in a remodelling vessel, not only the matrix but also the SMCs need to undergo structural adaptation. Surprisingly little is known on the adaptation of SMC contractile properties in the vasculature. The purpose of this review is to explore this SMC plasticity in the context of vascular remodelling. While not much work on this has been carried out on blood vessels, SMC plasticity is more extensively studied on other hollow structures such as airway and bladder. We therefore include studies on bladder and airway SMCs because of their possible relevance for vascular SMC behaviour. Here, plasticity is thought to form an adaptation allowing maintained function despite large volume changes. In blood vessels, the general match of active and passive diameter-tension relations suggests that SMC plasticity is part of normal vascular physiological adaptation. Vascular SMCs display similar processes and forms of adaptation as seen in nonvascular SMCs. This may become particularly relevant under strong vasoconstriction, when inward cytoskeletal adaptation possibly prevents immediate full dilation. This may contribute to structural inward remodelling as seen in hypertension and flow reduction.
Topics: Airway Remodeling; Airway Resistance; Animals; Biomechanical Phenomena; Blood Vessels; Cytoskeleton; Humans; Microcirculation; Microvessels; Muscle Tonus; Muscle, Smooth; Muscle, Smooth, Vascular; Respiratory System; Urinary Bladder; Vascular Resistance; Vasoconstriction; Vasodilation
PubMed: 21902815
DOI: 10.1111/j.1742-7843.2011.00794.x -
Journal of Muscle Research and Cell... Dec 2012The thin filaments of differentiated smooth muscle cells are composed of actin and tropomyosin isoforms and numerous ancillary actin-binding proteins that assemble... (Review)
Review
The thin filaments of differentiated smooth muscle cells are composed of actin and tropomyosin isoforms and numerous ancillary actin-binding proteins that assemble together into distinct thin filament classes. These different filament classes are segregated in smooth muscle cells into structurally and functionally separated contractile and cytoskeletal cellular domains. Typically, thin filaments in smooth muscle cells have been considered to be relatively stable structures like those in striated cells. However, recent efforts have shown that smooth muscle thin filaments indeed are dynamic and that remodeling of the actin cytoskeleton, in particular, regulates smooth muscle function. Thus, the cytoskeleton of differentiated smooth muscle cells appears to function midway between that of less dynamic striated muscle cells and that of very plastic proliferative cells such as fibroblasts. Michael and Kate Bárány keenly followed and participated in some of these studies, consistent with their broad interest in actin function and smooth muscle mechanisms. As a way of honoring the memory of these two pioneer members of the muscle research community, we review data on distribution and remodeling of thin filaments in smooth muscle cells, one of the many research topics that intrigued them.
Topics: Actins; Animals; Cytoskeleton; Humans; Models, Molecular; Molecular Structure; Muscle Contraction; Muscle, Smooth
PubMed: 22311558
DOI: 10.1007/s10974-012-9283-z -
Skeletal Muscle 2016The esophagus functions to transport food from the oropharyngeal region to the stomach via waves of peristalsis and transient relaxation of the lower esophageal... (Review)
Review
The esophagus functions to transport food from the oropharyngeal region to the stomach via waves of peristalsis and transient relaxation of the lower esophageal sphincter. The gastrointestinal tract, including the esophagus, is ensheathed by the muscularis externa (ME). However, while the ME of the gastrointestinal tract distal to the esophagus is exclusively smooth muscle, the esophageal ME of many vertebrate species comprises a variable amount of striated muscle. The esophageal ME is initially composed only of smooth muscle, but its developmental maturation involves proximal-to-distal replacement of smooth muscle with striated muscle. This fascinating phenomenon raises two important questions: what is the developmental origin of the striated muscle precursor cells, and what are the cellular and morphogenetic mechanisms underlying the process? Studies addressing these questions have provided controversial answers. In this review, we discuss the development of ideas in this area and recent work that has shed light on these issues. A working model has emerged that should permit deeper understanding of the role of ME development and maturation in esophageal disorders and in the functional and evolutionary underpinnings of the variable degree of esophageal striated myogenesis in vertebrate species.
Topics: Animals; Esophagus; Humans; Models, Biological; Muscle Development; Muscle Fibers, Skeletal; Muscle, Smooth; Muscle, Striated; Myoblasts; Myocytes, Smooth Muscle
PubMed: 27504178
DOI: 10.1186/s13395-016-0099-1 -
American Journal of Physiology. Heart... Oct 2018Hypoxic preconditioning, the protective effect of brief, intermittent hypoxic or ischemic episodes on subsequent more severe hypoxic episodes, has been known for 30 yr... (Review)
Review
Hypoxic preconditioning, the protective effect of brief, intermittent hypoxic or ischemic episodes on subsequent more severe hypoxic episodes, has been known for 30 yr from studies on cardiac muscle. The concept of hypoxic preconditioning has expanded; excitingly, organs beyond the heart, including the brain, liver, and kidney, also benefit. Preconditioning of vascular and visceral smooth muscles has received less attention despite their obvious importance to health. In addition, there has been no attempt to synthesize the literature in this field. Therefore, in addition to overviewing the current understanding of hypoxic conditioning, in the present review, we consider the role of blood vessels in conditioning and explore evidence for conditioning in other smooth muscles. Where possible, we have distinguished effects on myocytes from other cell types in the visceral organs. We found evidence of a pivotal role for blood vessels in conditioning and for conditioning in other smooth muscle, including the bladder, vascular myocytes, and gastrointestinal tract, and a novel response in the uterus of a hypoxic-induced force increase, which helps maintain contractions during labor. To date, however, there are insufficient data to provide a comprehensive or unifying mechanism for smooth muscles or visceral organs and the effects of conditioning on their function. This also means that no firm conclusions can be drawn as to how differences between smooth muscles in metabolic and contractile activity may contribute to conditioning. Therefore, we have suggested what may be general mechanisms of conditioning occurring in all smooth muscles and tabulated tissue-specific mechanistic findings and suggested ideas for further progress.
Topics: Animals; Blood Vessels; Humans; Ischemia; Ischemic Preconditioning; Muscle Contraction; Muscle, Smooth
PubMed: 29702009
DOI: 10.1152/ajpheart.00725.2017 -
Allergology International : Official... Sep 2006Airway remodeling in asthma has been recognized as structural changes of airways such as smooth muscle hypertrophy (an increase in size of airway smooth muscle cells)... (Review)
Review
Airway remodeling in asthma has been recognized as structural changes of airways such as smooth muscle hypertrophy (an increase in size of airway smooth muscle cells) and hyperplasia (an increase in the number of airway smooth muscle cells), thickening and fibrosis of sub-epithelial basement membrane, hypertrophy of bronchial glands, goblet cell hyperplasia, and thickening of airway epithelium. In these pathological changes, airway smooth muscle remodeling has been recognized as one of the most important factors related to in vitro and in vitro airway responsiveness and the severity of asthma. Both hypertrophy and hyperplasia have been shown in asthmatic airways by morphometrical analyses, although there is a wide variation in the contribution of each mechanism in each patient. Such changes could also be recognized as a phenotypic modulation of airway smooth muscle. On the background of airway smooth muscle remodeling, the existence of several contributing factors, such as inflammatory mediators, growth factors, cytokines, extra-cellular matrix proteins, and genetic factors have been suggested. On the other hand, recent studies revealed that airway smooth muscle could also be a source of inflammatory mediators promoting airway inflammation. In this article, the recent understanding in the mechanisms of airway smooth muscle remodeling in asthma, its relations to airway inflammation and airway physiology, and possible usefulness of early intervention with inhaled glucocorticoids have been discussed.
Topics: Animals; Asthma; Humans; Muscle, Smooth; Respiratory Physiological Phenomena
PubMed: 17075263
DOI: 10.2332/allergolint.55.235 -
The European Respiratory Journal Apr 1995In addition to its emerging immunodulatory properties, theophylline is a bronchodilator and also decreases mean pulmonary arterial pressure in vivo. The mechanism of... (Review)
Review
In addition to its emerging immunodulatory properties, theophylline is a bronchodilator and also decreases mean pulmonary arterial pressure in vivo. The mechanism of action of this drug remains controversial; adenosine antagonism, phosphodiesterase (PDE) inhibition and other actions have been advanced to explain its effectiveness in asthma. Cyclic adenosine monophosphate (AMP) and cyclic guanosine monophosphate (GMP) are involved in the regulation of smooth muscle tone, and the breakdown of these nucleotides is catalysed by multiple PDE isoenzymes. The PDE isoenzymes present in human bronchus and pulmonary artery have been identified, and the pharmacological actions of inhibitors of these enzymes have been investigated. Human bronchus and pulmonary arteries are relaxed by theophylline and by selective inhibitors of PDE III, while PDE IV inhibitors also relax precontracted bronchus and PDE V/I inhibitors relax pulmonary artery. There appears to be some synergy between inhibitors of PDE III and PDE IV in relaxing bronchus, and a pronounced synergy between PDE III and PDE V inhibitors in relaxing pulmonary artery. In neither tissue does 8-phenyltheophylline, a xanthine exhibiting adenosine antagonism but not PDE inhibition, cause any significant relaxation, implying that theophylline does not exert its actions through adenosine antagonism. The close correspondence of theophylline concentrations inhibiting bronchus or pulmonary artery PDE and those causing relaxation points towards PDE inhibition as the major mechanism of action of theophylline in smooth muscle relaxation.
Topics: Animals; Bronchi; Bronchodilator Agents; Cyclic AMP; Cyclic GMP; Humans; Muscle, Smooth; Muscle, Smooth, Vascular; Parasympatholytics; Phosphodiesterase Inhibitors; Pulmonary Artery; Theophylline
PubMed: 7664866
DOI: No ID Found