Mechanisms for the mechanical plasticity of tracheal smooth muscle

1995 ◽  
Vol 268 (5) ◽  
pp. C1267-C1276 ◽  
Author(s):  
S. J. Gunst ◽  
R. A. Meiss ◽  
M. F. Wu ◽  
M. Rowe
Keyword(s):  
Smooth Muscle ◽  
Stimulus Intensity ◽  
Isometric Force ◽  
Muscle Length ◽  
Muscle Stiffness ◽  
Force Development ◽  
Cross Bridges ◽  
High Level ◽  
Cellular Components ◽  
The Relationship

In smooth muscle tissues, the relationship between muscle or cell length and active force can be modulated by altering the cell or tissue length during stimulation. Mechanisms for this mechanical plasticity were investigated by measuring muscle stiffness during isometric contractions in which contractile force was graded by changing stimulus intensity or muscle length. Stiffness was significantly higher in contracted than in resting muscles at comparable forces; however, the relationship between stiffness and force during force development was curvilinear and independent of muscle length and stimulus intensity. This suggests that muscle stiffness during force development reflects properties of cellular components other than cross bridges which contribute to the series elasticity only during activation. During the tonic phase of isometric contraction, muscle stiffness increased while force remained constant. A step decrease in the length of a contracted muscle resulted in a high level of stiffness relative to force during isometric force redevelopment following the length step. We propose that the arrangement of the cytoskeleton can adjust to changes in the conformation of resting smooth muscle cells but that the organization of the cytoskeleton becomes more fixed upon contractile activation and is modulated very slowly during a sustained contraction. This may provide a mechanism for optimizing force development to the physical conformation of the cell at the time of activation.

Cooperative attachment of cross bridges predicts regulation of smooth muscle force by myosin phosphorylation

2004 ◽  
Vol 287 (3) ◽  
pp. C594-C602 ◽  
Author(s):  
Christopher M. Rembold ◽  
Robert L. Wardle ◽  
Christopher J. Wingard ◽  
Timothy W. Batts ◽  
Elaine F. Etter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Time Course ◽  
Muscle Force ◽  
Regulatory System ◽  
Force Development ◽  
Cross Bridge ◽  
Cross Bridges ◽  
The Relationship ◽  
Cooperative Activation

Serine 19 phosphorylation of the myosin regulatory light chain (MRLC) appears to be the primary determinant of smooth muscle force development. The relationship between MRLC phosphorylation and force is nonlinear, showing that phosphorylation is not a simple switch regulating the number of cycling cross bridges. We reexamined the MRLC phosphorylation-force relationship in slow, tonic swine carotid media; fast, phasic rabbit urinary bladder detrusor; and very fast, tonic rat anococcygeus. We found a sigmoidal dependence of force on MRLC phosphorylation in all three tissues with a threshold for force development of ∼0.15 mol Pi/mol MRLC. This behavior suggests that force is regulated in a highly cooperative manner. We then determined whether a model that employs both the latch-bridge hypothesis and cooperative activation could reproduce the relationship between Ser19-MRLC phosphorylation and force without the need for a second regulatory system. We based this model on skeletal muscle in which attached cross bridges cooperatively activate thin filaments to facilitate cross-bridge attachment. We found that such a model describes both the steady-state and time-course relationship between Ser19-MRLC phosphorylation and force. The model required both cooperative activation and latch-bridge formation to predict force. The best fit of the model occurred when binding of a cross bridge cooperatively activated seven myosin binding sites on the thin filament. This result suggests cooperative mechanisms analogous to skeletal muscle that will require testing.

Effects of initial length on intrinsic tone in guinea pig tracheal smooth muscle

1998 ◽  
Vol 275 (6) ◽  
pp. L1026-L1030 ◽  
Author(s):  
Martin Bard ◽  
Sergio Salmeron ◽  
Catherine Coirault ◽  
Francois-Xavier Blanc ◽  
Yves Lecarpentier
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Isometric Force ◽  
Muscle Length ◽  
Tracheal Smooth Muscle ◽  
Before And After ◽  
Active Nature ◽  
The Difference ◽  
Resting Tone ◽  
The Relationship

In the guinea pig, tracheal smooth muscle (TSM) exhibits intrinsic tone (IT). The active nature of IT suggests that it could be influenced by muscle length and load. In the guinea pig, IT is entirely suppressed by the cyclooxygenase inhibitor indomethacin. IT could be measured as the difference between resting tone before and after indomethacin addition. We examined, in electrically stimulated TSM strips ( n= 9), the influence of initial muscle length ( L i) on IT, the relationship between IT and the maximum extent of relaxation (ΔF1), and the influence of indomethacin on active isometric force. When L i decreased from 100 to 75% of optimal L i, there was a significant decrease in IT (from 12.0 ± 0.2 to 5.3 ± 0.1 mN; P < 0.001). Over the range of L i studied, ΔF1 underestimated the amount of IT, but there was a close linear relationship between ΔF1 and IT ( r = 0.9). Compared with the basal state, indomethacin increased active isometric force (from 9.5 ± 1.0 to 19.7 ± 2.0 mN at optimal L i; P < 0.001) and induced its length dependency. In guinea pig TSM, L i was an important determinant of IT.

scholarly journals Could an increase in airway smooth muscle shortening velocity cause airway hyperresponsiveness?

2011 ◽  
Vol 300 (1) ◽  
pp. L121-L131 ◽  
Author(s):  
Sharon R. Bullimore ◽  
Sana Siddiqui ◽  
Graham M. Donovan ◽  
James G. Martin ◽  
James Sneyd ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Isometric Force ◽  
Muscle Length ◽  
Shortening Velocity ◽  
Bridge Model ◽  
Generating Capacity ◽  
Cross Bridges

Airway hyperresponsiveness (AHR) is a characteristic feature of asthma. It has been proposed that an increase in the shortening velocity of airway smooth muscle (ASM) could contribute to AHR. To address this possibility, we tested whether an increase in the isotonic shortening velocity of ASM is associated with an increase in the rate and total amount of shortening when ASM is subjected to an oscillating load, as occurs during breathing. Experiments were performed in vitro using 27 rat tracheal ASM strips supramaximally stimulated with methacholine. Isotonic velocity at 20% isometric force (Fiso) was measured, and then the load on the muscle was varied sinusoidally (0.33 ± 0.25 Fiso, 1.2 Hz) for 20 min, while muscle length was measured. A large amplitude oscillation was applied every 4 min to simulate a deep breath. We found that: 1) ASM strips with a higher isotonic velocity shortened more quickly during the force oscillations, both initially ( P < 0.001) and after the simulated deep breaths ( P = 0.002); 2) ASM strips with a higher isotonic velocity exhibited a greater total shortening during the force oscillation protocol ( P < 0.005); and 3) the effect of an increase in isotonic velocity was at least comparable in magnitude to the effect of a proportional increase in ASM force-generating capacity. A cross-bridge model showed that an increase in the total amount of shortening with increased isotonic velocity could be explained by a change in either the cycling rate of phosphorylated cross bridges or the rate of myosin light chain phosphorylation. We conclude that, if asthma involves an increase in ASM velocity, this could be an important factor in the associated AHR.

Changes of tracheal smooth muscle stiffness during an isotonic contraction

1989 ◽  
Vol 256 (2) ◽  
pp. C341-C350 ◽  
Author(s):  
C. Y. Seow ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Muscle Length ◽  
Fixed Time ◽  
Isometric Tension ◽  
Muscle Stiffness ◽  
Tracheal Smooth Muscle ◽  
Isotonic Contraction ◽  
Small Force ◽  
Cross Bridges ◽  
Contraction And Relaxation

Stiffness of the series elastic component (SEC) of canine tracheal smooth muscle in isotonic contraction and relaxation was measured by applying small force perturbations to the muscle and measuring the resulting length perturbations. The quick, elastic length transient was taken as the change in length of the SEC (delta L). The force perturbation was a train of 10-Hz rectangular force waves varying from 0 to 10% maximum isometric tension (Po) in magnitude (delta P = 10% Po). Stiffness of the SEC was estimated by the ratio delta P/delta L. The change in SEC stiffness with respect to the change in muscle length was further studied by obtaining the stress-strain curves of the SEC at different muscle lengths using the load-clamping method. The clamps were applied at a fixed time (10 s after stimulation). Length of the muscle 10 s after contraction was controlled by the magnitude of the isotonic afterload. It was found that the apparent SEC stiffness increased as muscle length decreased. This stiffness increase is not likely due to an increase in the number of attached cross bridges, but it is probably due to the gradual diminution of the SEC length itself during muscle shortening.

scholarly journals Characterization of cross-bridge elasticity and kinetics of cross-bridge cycling during force development in single smooth muscle cells.

1988 ◽  
Vol 91 (6) ◽  
pp. 761-779 ◽  
Author(s):  
D M Warshaw ◽  
D D Rees ◽  
F S Fay
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Isometric Force ◽  
Force Development ◽  
Cross Bridge ◽  
Tension Recovery ◽  
Length Changes ◽  
Cross Bridges ◽  
Initial Force ◽  
Kinetics Of

Force development in smooth muscle, as in skeletal muscle, is believed to reflect recruitment of force-generating myosin cross-bridges. However, little is known about the events underlying cross-bridge recruitment as the muscle cell approaches peak isometric force and then enters a period of tension maintenance. In the present studies on single smooth muscle cells isolated from the toad (Bufo marinus) stomach muscularis, active muscle stiffness, calculated from the force response to small sinusoidal length changes (0.5% cell length, 250 Hz), was utilized to estimate the relative number of attached cross-bridges. By comparing stiffness during initial force development to stiffness during force redevelopment immediately after a quick release imposed at peak force, we propose that the instantaneous active stiffness of the cell reflects both a linearly elastic cross-bridge element having 1.5 times the compliance of the cross-bridge in frog skeletal muscle and a series elastic component having an exponential length-force relationship. At the onset of force development, the ratio of stiffness to force was 2.5 times greater than at peak isometric force. These data suggest that, upon activation, cross-bridges attach in at least two states (i.e., low-force-producing and high-force-producing) and redistribute to a steady state distribution at peak isometric force. The possibility that the cross-bridge cycling rate was modulated with time was also investigated by analyzing the time course of tension recovery to small, rapid step length changes (0.5% cell length in 2.5 ms) imposed during initial force development, at peak force, and after 15 s of tension maintenance. The rate of tension recovery slowed continuously throughout force development following activation and slowed further as force was maintained. Our results suggest that the kinetics of force production in smooth muscle may involve a redistribution of cross-bridge populations between two attached states and that the average cycling rate of these cross-bridges becomes slower with time during contraction.

Oxytocin-mediated recruitment of slowly cycling cross bridges and isometric force in rat myometrium

1996 ◽  
Vol 270 (2) ◽  
pp. E203-E208
Author(s):  
A. L. Ruzycky ◽  
B. T. Ameredes
Keyword(s):  
Isometric Force ◽  
Additional Stress ◽  
Shortening Velocity ◽  
Cycling Rate ◽  
Quick Release ◽  
Cross Bridge ◽  
Cross Bridges ◽  
Unit Stress ◽  
Release Method ◽  
The Relationship

The relationship between cross-bridge cycling rate and isometric stress was investigated in rat myometrium. Stress production by myometrial strips was measured under resting, K+ depolarization, and oxytocin-stimulated conditions. Cross-bridge cycling rates were determined from measurements of maximal unloaded shortening velocity, using the quick-release method. Force redevelopment after the quick release was used as an index of cross-bridge attachment. With maximal K+ stimulation, stress increased with increased cross-bridge cycling (+76%; P < 0.05) and attached cross bridges (+112%; P < 0.05). Addition of oxytocin during K+ stimulation further increased stress (+30%; P < 0.05). With this force component, the cross-bridge cycling rate decreased (-60%; P < 0.05) similar to that under resting conditions. Attached cross-bridges did not increase with this additional stress. The results suggest two distinct mechanisms mediating myometrial contractions. One requires elevated intracellular calcium and rapidly cycling cross bridges. The other mechanism may be independent of calcium and appears to be mediated by slowly cycling cross bridges, supporting greater unit stress.

The effects of pH on force and stiffness development in mouse muscles

1987 ◽  
Vol 65 (8) ◽  
pp. 1798-1801 ◽  
Author(s):  
J. M. Renaud ◽  
R. B. Stein ◽  
T. Gordon
Keyword(s):  
High Frequency ◽  
Small Amplitude ◽  
Force Production ◽  
Muscle Length ◽  
Low Ph ◽  
Muscle Stiffness ◽  
Average Force ◽  
Cross Bridge ◽  
Effects Of Ph ◽  
Cross Bridges

Changes in force and stiffness during contractions of mouse extensor digitorum longus and soleus muscles were measured over a range of extracellular pH from 6.4 to 7.4. Muscle stiffness was measured using small amplitude (<0.1% of muscle length), high frequency (1.5 kHz) oscillations in length. Twitch force was not significantly affected by changes in pH, but the peak force during repetitive stimulation (2, 3, and 20 pulses) was decreased significantly as the pH was reduced. Changes in muscle stiffness with pH were in the same direction, but smaller in extent. If the number of attached cross-bridges in the muscle can be determined from the measurement of small amplitude, high frequency muscle stiffness, then these findings suggest that (a) the number of cross-bridges between thick and thin filaments declines in low pH and (b) the average force per cross-bridge also declines in low pH. The decline in force per cross-bridge could arise from a reduction in the ability of cross-bridges to generate force during their state of active force production and (or) in an increased percentage of bonds in a low force, "rigor" state.

scholarly journals Influence of muscle length on work from trabecular muscle of frog atrium and ventricle.

1995 ◽  
Vol 198 (10) ◽  
pp. 2221-2227 ◽  
Author(s):  
D A Syme ◽  
R K Josephson
Keyword(s):  
Isometric Force ◽  
Muscle Length ◽  
Work Capacity ◽  
Linear Increase ◽  
Ventricular Muscle ◽  
Work Output ◽  
Loop Technique ◽  
Work Done ◽  
The Relationship ◽  
Work Loop

The work capacity of segments of atrial and ventricular muscle from the frog Rana pipiens was measured as a function of muscle length using the work loop technique. Both the work done during shortening and the work required to re-lengthen the muscle after shortening increased with muscle length. Net work increased with length up to a maximum, beyond which work declined. The optimum sarcomere length for work output was 2.5-2.6 microns for both atrial and ventricular muscle. Isometric force increased with muscle length to lengths well beyond the optimum for work output. Thus, the decline in work at long lengths is not simply a consequence of a reduction in the capacity of heart muscle to generate force. It is proposed that it is the non-linear increase in work required to re-lengthen muscle with increasing muscle length which limits net work output and leads to a maximum in the relationship between net work and muscle length. Extension of the results from muscle strips to intact hearts suggests that the work required to fill the ventricle exceeds that available from atrial muscle at all but rather short ventricular muscle lengths.

Regulation of shortening velocity by cross-bridge phosphorylation in smooth muscle

1988 ◽  
Vol 255 (1) ◽  
pp. C86-C94 ◽  
Author(s):  
C. M. Hai ◽  
R. A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Shortening Velocity ◽  
Internal Load ◽  
Cross Bridge ◽  
Bridge Model ◽  
The Family ◽  
Cross Bridges ◽  
Latch State ◽  
The Relationship ◽  
State Stress

We have proposed a model that incorporates a dephosphorylated "latch bridge" to explain the mechanics and energetics of smooth muscle. Cross-bridge phosphorylation is proposed as a prerequisite for cross-bridge attachment and rapid cycling. Features of the model are 1) myosin light chain kinase and phosphatase can act on both free and attached cross bridges, 2) dephosphorylation of an attached phosphorylated cross bridge produces a noncycling "latch bridge," and 3) latch bridges have a slow detachment rate. This model quantitatively predicts the latch state: stress maintenance with reduced phosphorylation, cross-bridge cycling rates, and ATP consumption. In this study, we adapted A. F. Huxley's formulation of crossbridge cycling (A. F. Huxley, Progr. Biophys. Mol. Biol. 7: 255-318, 1957) to the latch-bridge model to predict the relationship between isotonic shortening velocity and phosphorylation. The model successfully predicted the linear dependence of maximum shortening velocity at zero external load (V0) on phosphorylation, as well as the family of stress-velocity curves determined at different times during a contraction when phosphorylation values varied. The model implies that it is unnecessary to invoke an internal load or multiple regulatory mechanisms to explain regulation of V0 in smooth muscle.

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