Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
Syyong HT, Raqeeb A, Paré PD, Seow CY. Time course of isotonic shortening and the underlying contraction mechanism in airway smooth muscle. J Appl Physiol 111: 642-656, 2011. First published June 2, 2011; doi:10.1152/japplphysiol.00085.2011.-Although the structure of the contractile unit in smooth muscle is poorly understood, some of the mechanical properties of the muscle suggest that a sliding-filament mechanism, similar to that in striated muscle, is also operative in smooth muscle. To test the applicability of this mechanism to smooth muscle function, we have constructed a mathematical model based on a hypothetical structure of the smooth muscle contractile unit: a side-polar myosin filament sandwiched by actin filaments, each attached to the equivalent of a Z disk. Model prediction of isotonic shortening as a function of time was compared with data from experiments using ovine tracheal smooth muscle. After equilibration and establishment of in situ length, the muscle was stimulated with ACh (100 M) until force reached a plateau. The muscle was then allowed to shorten isotonically against various loads. From the experimental records, length-force and force-velocity relationships were obtained. Integration of the hyperbolic force-velocity relationship and the linear length-force relationship yielded an exponential function that approximated the time course of isotonic shortening generated by the modeled sliding-filament mechanism. However, to obtain an accurate fit, it was necessary to incorporate a viscoelastic element in series with the sliding-filament mechanism. The results suggest that a large portion of the shortening is due to filament sliding associated with muscle activation and that a small portion is due to continued deformation associated with an element that shows viscoelastic or power-law creep after a step change in force. mathematical model; contractile unit; sliding-filament mechanism THE STRUCTURE OF THE CONTRACTILE unit in smooth muscle is unknown, despite the common belief that the cycling-crossbridge/sliding-filament mechanism of contraction, which operates in striated muscle, is also responsible for smooth muscle contraction. The predominant model for the sarcomere-equivalent contractile unit in smooth muscle is a side-polar myosin (thick) filament sandwiched by two oppositely oriented actin (thin) filaments, each attached to a dense body that is believed to function like a Z disk in striated muscle (18,21,27), as shown in Fig. 1. An important assumption associated with the model is that the sliding of the thick and thin filaments relative to each other is caused by repetitive interaction of the myosin heads (cross bridges) of the thick filament with the thin filaments, in the same manner described for striated muscle (22,23). Such a cross-bridge mechanism for smooth muscle myosin has been observed in experiments where the interaction of isolated individual myosin heads with thin filaments was visualized and quantified directly (14, 15, 28). As predicted by Huxley's 1957 model (22), the ...
Syyong HT, Raqeeb A, Paré PD, Seow CY. Time course of isotonic shortening and the underlying contraction mechanism in airway smooth muscle. J Appl Physiol 111: 642-656, 2011. First published June 2, 2011; doi:10.1152/japplphysiol.00085.2011.-Although the structure of the contractile unit in smooth muscle is poorly understood, some of the mechanical properties of the muscle suggest that a sliding-filament mechanism, similar to that in striated muscle, is also operative in smooth muscle. To test the applicability of this mechanism to smooth muscle function, we have constructed a mathematical model based on a hypothetical structure of the smooth muscle contractile unit: a side-polar myosin filament sandwiched by actin filaments, each attached to the equivalent of a Z disk. Model prediction of isotonic shortening as a function of time was compared with data from experiments using ovine tracheal smooth muscle. After equilibration and establishment of in situ length, the muscle was stimulated with ACh (100 M) until force reached a plateau. The muscle was then allowed to shorten isotonically against various loads. From the experimental records, length-force and force-velocity relationships were obtained. Integration of the hyperbolic force-velocity relationship and the linear length-force relationship yielded an exponential function that approximated the time course of isotonic shortening generated by the modeled sliding-filament mechanism. However, to obtain an accurate fit, it was necessary to incorporate a viscoelastic element in series with the sliding-filament mechanism. The results suggest that a large portion of the shortening is due to filament sliding associated with muscle activation and that a small portion is due to continued deformation associated with an element that shows viscoelastic or power-law creep after a step change in force. mathematical model; contractile unit; sliding-filament mechanism THE STRUCTURE OF THE CONTRACTILE unit in smooth muscle is unknown, despite the common belief that the cycling-crossbridge/sliding-filament mechanism of contraction, which operates in striated muscle, is also responsible for smooth muscle contraction. The predominant model for the sarcomere-equivalent contractile unit in smooth muscle is a side-polar myosin (thick) filament sandwiched by two oppositely oriented actin (thin) filaments, each attached to a dense body that is believed to function like a Z disk in striated muscle (18,21,27), as shown in Fig. 1. An important assumption associated with the model is that the sliding of the thick and thin filaments relative to each other is caused by repetitive interaction of the myosin heads (cross bridges) of the thick filament with the thin filaments, in the same manner described for striated muscle (22,23). Such a cross-bridge mechanism for smooth muscle myosin has been observed in experiments where the interaction of isolated individual myosin heads with thin filaments was visualized and quantified directly (14, 15, 28). As predicted by Huxley's 1957 model (22), the ...
Excessive narrowing of the airways due to airway smooth muscle (ASM) contraction is a major cause of asthma exacerbation. ASM is therefore a direct target for many drugs used in asthma therapy. The contractile mechanism of smooth muscle is not entirely clear. A major advance in the field in the last decade was the recognition and appreciation of the unique properties of smooth muscle--mechanical and structural plasticity, characterized by the muscle's ability to rapidly alter the structure of its contractile apparatus and cytoskeleton and adapt to the mechanically dynamic environment of the lung. This article describes a possible mechanism for smooth muscle to adapt and function over a large length range by adding or subtracting contractile units in series spanning the cell length; it also describes a mechanism by which actin-myosin-actin connectivity might be influenced by thin and thick filament lengths, thus altering the muscle response to mechanical perturbation. The new knowledge is extremely useful for our understanding of ASM behavior in the lung and could provide new and more effective targets for drugs aimed at relaxing the muscle or keeping the muscle from excessive shortening in the asthmatic airways.
In this manuscript we discuss the interaction of the lung parenchyma and the airways as well as the physiological and pathophysiological significance of this interaction. These two components of the respiratory organ can be thought of as two independent elastic structures but in fact the mechanical properties of one influence the behavior of the other. Traditionally the interaction has focused on the effects of the lung on the airways but there is good evidence that the opposite is also true, i.e., that the mechanical properties of the airways influence the elastic properties of the parenchyma. The interplay between components of the respiratory system including the airways, parenchyma and vasculature is often referred to as “interdependence.” This interdependence transmits the elastic recoil of the lung to create an effective pressure that dilates the airways as transpulmonary pressure and lung volume increase. By using a continuum mechanics analysis of the lung parenchyma, it is possible to predict the effective pressure between the airways and parenchyma, and these predictions can be empirically evaluated. Normal airway caliber is maintained by this pressure in the adventitial interstitium of the airway, and it counteracts airway compression during forced expiration as well as the ability of airway smooth muscle to narrow airways. Interdependence has physiological and pathophysiological significance. Weakening of the forces of interdependence contributes to airway dysfunction and gas exchange impairment in acute and chronic airway diseases including asthma and emphysema.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.