scholarly journals Adaptation of the length-active tension relationship in rabbit detrusor

2009 ◽  
Vol 297 (4) ◽  
pp. F1119-F1128 ◽  
Author(s):  
John E. Speich ◽  
Atheer M. Almasri ◽  
Hersch Bhatia ◽  
Adam P. Klausner ◽  
Paul H. Ratz
Keyword(s):  
Smooth Muscles ◽  
Muscle Length ◽  
Strain History ◽  
Detrusor Smooth Muscle ◽  
Active Tension ◽  
Passive Stiffness ◽  
Vascular Smooth Muscles ◽  
Length Changes ◽  
Adjustable Passive Stiffness ◽  
First Time

Studies have shown that the length-tension ( L-T) relationships in airway and vascular smooth muscles are dynamic and can adapt to length changes over a period of time. Our prior studies have shown that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that can shift along the length axis as a function of strain history and activation history. The present study demonstrates that the active L-T curve for DSM is also dynamic and that the peak active tension produced at a particular muscle length is a function of both strain and activation history. More specifically, this study reveals that the active L-T relationship, or curve, does not have a unique peak tension value with a single ascending and descending limb, but instead reveals that multiple ascending and descending limbs can be exhibited in the same DSM strip. This study also demonstrates that for DSM strips not stretched far enough to reveal a descending limb, the peak active tension produced by a maximal KCl-induced contraction at a short, passively slack muscle length of 3 mm was reduced by 58.6 ± 4.1% ( n = 1 5) following stretches to and contractions at threefold the original muscle length, 9 mm. Moreover, five subsequent contractions at the short muscle length displayed increasingly greater tension; active tension produced by the sixth contraction was 91.5 ± 9.1% of that produced by the prestretch contraction at that length. Together, these findings indicate for the first time that DSM exhibits length adaptation, similar to vascular and airway smooth muscles. In addition, our findings demonstrate that preconditioning, APS and adaptation of the active L-T curve can each impact the maximum total tension observed at a particular DSM length.

scholarly journals Rhythmic contraction generates adjustable passive stiffness in rabbit detrusor

2010 ◽  
Vol 108 (3) ◽  
pp. 544-553 ◽  
Author(s):  
Atheer M. Almasri ◽  
Paul H. Ratz ◽  
Hersch Bhatia ◽  
Adam P. Klausner ◽  
John E. Speich
Keyword(s):  
Kinase Inhibitor ◽  
Smooth Muscles ◽  
Physiological Role ◽  
Passive Tension ◽  
Passive Stiffness ◽  
Vascular Smooth Muscles ◽  
Rhythmic Contraction ◽  
Length Changes ◽  
Changes Over Time ◽  
Adjustable Passive Stiffness

The length-tension ( L-T) relationships in airway and vascular smooth muscles have been shown to adapt with length changes over time. Our prior studies have shown that the active and passive L-T relationships in rabbit detrusor smooth muscle (DSM) can adapt and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that is a function of strain and activation history. The present study demonstrates that passive tension due to APS can represent a substantial fraction of total tension over a broad length range. Our previous studies have shown that maximal KCl-induced contractions at short muscle lengths generate APS that is revealed by increased pseudo-steady-state passive tension at longer lengths compared with previous measurements at those lengths. The objective of the present study was to determine the mechanisms involved in APS generation. Increasing the number of KCl-induced contractions or the duration of a contraction increased the amount of APS generated. Furthermore, a fraction of APS was restored in calcium-free solution and was sensitive to the general serine and threonine protein kinase inhibitor staurosporine. Most importantly, rhythmic contraction (RC) generated APS, and because RC occurs spontaneously in human bladder, a physiological role for RC was potentially identified.

Adjustable passive length-tension curve in rabbit detrusor smooth muscle

2007 ◽  
Vol 102 (5) ◽  
pp. 1746-1755 ◽  
Author(s):  
John E. Speich ◽  
Christopher Dosier ◽  
Lindsey Borgsmiller ◽  
Kevin Quintero ◽  
Harry P. Koo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Strain Softening ◽  
Muscle Length ◽  
Strain History ◽  
Total Force ◽  
Detrusor Smooth Muscle ◽  
Passive Force ◽  
Passive Stiffness ◽  
Active Force ◽  
Length Changes

Until the 1990s, the passive and active length-tension ( L-T) relationships of smooth muscle were believed to be static, with a single passive force value and a single maximum active force value for each muscle length. However, recent studies have demonstrated that the active L-T relationship in airway smooth muscle is dynamic and adapts to length changes over a period of time. Furthermore, our prior work showed that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that in addition to viscoelastic behavior, DSM displays strain-softening behavior characterized by a loss of passive stiffness at shorter lengths following a stretch to a new longer length. This loss of passive stiffness appears to be irreversible when the muscle is not producing active force and during submaximal activation but is reversible on full muscle activation, which indicates that the stiffness component of passive force lost to strain softening is adjustable in DSM. The present study demonstrates that the passive L-T curve for DSM is not static and can shift along the length axis as a function of strain history and activation history. This study also demonstrates that adjustable passive stiffness (APS) can modulate total force (35% increase) for a given muscle length, while active force remains relatively unchanged (4% increase). This finding suggests that the structures responsible for APS act in parallel with the contractile apparatus, and the results are used to further justify the configuration of modeling elements within our previously proposed mechanical model for APS.

Calcium-dependent resistance to stretch and stress relaxation in resting smooth muscles

1976 ◽  
Vol 231 (5) ◽  
pp. 1501-1508 ◽  
Author(s):  
MJ Siegman ◽  
TM Butler ◽  
SU Mooers ◽  
RE Davies
Keyword(s):  
Stress Relaxation ◽  
Smooth Muscles ◽  
Muscle Length ◽  
Taenia Coli ◽  
Tetraacetic Acid ◽  
Active Tension ◽  
Tension Development ◽  
Calcium Dependent ◽  
Mechanical Responses ◽  
State Force

Mechanical responses to stretch and length-tension relations were examined in rabbit taenia coli, mesenteric vein, aorta, and myometrium and in guinea pig taenia coli made atonic by incubation in Krebs-bicarbonate solution at 20-22 degrees C. When stretched 10% of the length at which maximum active tension is observed (Lo) in 0.5 s, the muscles showed a transient large force (resistance to stretch) that decayed to a new constant level within minutes (stress relaxation). The resistance to stretch decreased markedly in Ca2+-free [disodium ethylene glycolbis-(beta-aminoethylether)-N,N-tetraacetic acid (EGTA)] Krebs but was restored in normal Krebs solution. Calcium removal did not affect the passive length-tension curve. The absence of Ca2+ did not change the steady-state force maintained by the muscle; thus stretch resistance was not due to tone. Blockade of Ca2+ influx associated with electrical activity with 5-[3,4-dimethoxyphenethyl)methylamino]-2-(3,4,5-trimethoxyphenyl-2-isoprop ylvaleronitrile (D-600) and of Ca2+ release from intracellular sites with thymol (1 mM) completely blocked contraction but did not alter the responses to stretch, thus dissociating the responses to stretch from these processes and tension development. The Ca2+-dependent stress relaxation showed a dependence on muscle length similar to that for active tension development. Except at long muscle lengths, where connective tissue markedly affects length-tension relations, most of the "viscoelasticity" of these smooth muscles is dependent on calcium and may be largely due to the straining of crossbridges that are attached, but not generating a net force, in the resting state.

Transient responses and continuous behavior of active smooth muscle during controlled stretches

1982 ◽  
Vol 242 (3) ◽  
pp. C146-C158 ◽  
Author(s):  
R. A. Meiss
Keyword(s):  
Steady State ◽  
Smooth Muscles ◽  
Muscle Length ◽  
Initial Slope ◽  
Stretch Rate ◽  
Rate Dependent ◽  
Upward Slope ◽  
Length Changes ◽  
State Force ◽  
The Relationship

Controlled length changes were imposed on mesotubarium superius and ovarian ligament smooth muscles from the reproductive tracts of female rabbits in constant estrus. Stretches of up to 35% of the muscle length were applied during isometric contraction, relaxation, and steady-state force levels. Force was continuously monitored and was plotted as a function of length. During constant velocity stretches there was an initial steep rise in force, a rapid downward deviation from the initial slope, and a long region with a constant upward slope. Stretches made during contraction showed smaller initial rises in force and steeper linear portions than did identical comparison stretches made during relaxation. The value of the slope was independent of the prior developed force, but it did depend on whether the muscle was contracting or relaxing. During contraction and steady-state force levels, the slope was independent of the stretch rate, but it was strongly rate dependent during relaxation. Changes in the stretch rate during stretch caused associated changes in muscle force; the relationship was curvilinear and was exaggerated during relaxation. The findings are placed in the context of a sliding-filament--cross-bridge hypothesis.

scholarly journals Adjustable passive stiffness in mouse bladder: regulated by Rho kinase and elevated following partial bladder outlet obstruction

2012 ◽  
Vol 302 (8) ◽  
pp. F967-F976 ◽  
Author(s):  
John E. Speich ◽  
Jordan B. Southern ◽  
Sheree Henderson ◽  
Cameron W. Wilson ◽  
Adam P. Klausner ◽  
...  
Keyword(s):  
Bladder Outlet Obstruction ◽  
Bladder Wall ◽  
Rho Kinase ◽  
Outlet Obstruction ◽  
Prostaglandin E ◽  
Passive Stiffness ◽  
Regulatory Pathways ◽  
Partial Bladder Outlet Obstruction ◽  
Length Changes ◽  
Adjustable Passive Stiffness

Detrusor smooth muscle (DSM) contributes to bladder wall tension during filling, and bladder wall deformation affects the signaling system that leads to urgency. The length-passive tension ( L-Tp) relationship in rabbit DSM can adapt with length changes over time and exhibits adjustable passive stiffness (APS) characterized by a L-Tpcurve that is a function of both activation and strain history. Muscle activation with KCl, carbachol (CCh), or prostaglandin E2at short muscle lengths can increase APS that is revealed by elevated pseudo-steady-state Tpat longer lengths compared with prior Tpmeasurements at those lengths, and APS generation is inhibited by the Rho Kinase (ROCK) inhibitor H-1152. In the current study, mouse bladder strips exhibited both KCl- and CCh-induced APS. Whole mouse bladders demonstrated APS which was measured as an increase in pressure during passive filling in calcium-free solution following CCh precontraction compared with pressure during filling without precontraction. In addition, CCh-induced APS in whole mouse bladder was inhibited by H-1152, indicating that ROCK activity may regulate bladder compliance during filling. Furthermore, APS in whole mouse bladder was elevated 2 wk after partial bladder outlet obstruction, suggesting that APS may be relevant in diseases affecting bladder mechanics. The presence of APS in mouse bladder will permit future studies of APS regulatory pathways and potential alterations of APS in disease models using knockout transgenetic mice.

Mechanisms of length history-dependent tension in an ionic model of the cardiac myocyte

1998 ◽  
Vol 274 (3) ◽  
pp. H1032-H1040 ◽  
Author(s):  
Wolfgang F. Bluhm ◽  
Wilbur Y. W. Lew ◽  
Alan Garfinkel ◽  
Andrew D. McCulloch
Keyword(s):  
Cardiac Myocyte ◽  
Muscle Length ◽  
Step Change ◽  
Ventricular Myocyte ◽  
Active Tension ◽  
Leak Current ◽  
Slow Increase ◽  
Ionic Model ◽  
Length Changes ◽  
Induced Changes

The ionic model of the ventricular myocyte developed by Luo and Rudy ( Circ. Res. 74: 1071–1096, 1994) was used to investigate potential mechanisms of the slow changes in stress (SCS) that follow step changes in muscle length. A step change in myofilament sensitivity alone caused an immediate increase in active tension, but no SCS. The effects of additional step changes in the parameters of sarcolemmal ion fluxes were examined for each ion flux in the model. Changes in the coefficients of Ca2+ or K+ channels did not produce SCS. SCS was produced by step changes in parameters of the Na+-K+pump or the Na+ leak current. This simulated mechanism was mediated through a slow increase in intracellular Na+ concentration and a resulting increase in systolic Ca2+ entry through the Na+/Ca2+exchanger. The model reproduced the effects of several experimental interventions such as sarcoplasmic reticulum Ca2+ depletion, “diastolic” length changes, and changes in extracellular Ca2+. Thus SCS in cardiac muscle may be caused by length-induced changes in sarcolemmal Na+ fluxes.

Effect of muscle length on the in vitro comparison of femoral arteries before and after endotoxin shock

1993 ◽  
Vol 265 (4) ◽  
pp. H1160-H1166 ◽  
Author(s):  
Z. Zhou ◽  
J. M. Price ◽  
E. T. Sutton ◽  
C. H. Baker
Keyword(s):  
Dose Response ◽  
Muscle Length ◽  
Endotoxin Shock ◽  
Active Tension ◽  
Passive Stiffness ◽  
Femoral Arteries ◽  
Resting Tension ◽  
Before And After ◽  
Tension Experiments

Control and endotoxin-treated femoral arteries were compared in vitro for the effect of muscle length. Rats were anesthetized with pentobarbital, and endotoxin (6 mg/kg) was infused for 1 h. A control ring before endotoxin treatment and a ring after endotoxin treatment (blood pressure = 40 mmHg) were excised from the contralateral artery for length-tension and dose-response experiments with phenylephrine. The initial length for resting tension (Li) was shorter for endotoxic rings (1.23 +/- 0.01 vs. 1.41 +/- 0.02 mm in control), but the length of maximum active tension (Lmax) was the same. In length-tension experiments the values for active tension (6.36 +/- 0.61 vs. 4.06 +/- 0.60 x 10(3) dyn/cm), preload at Lmax (1,333 +/- 204 vs. 733 +/- 146 mg), and passive stiffness were increased after endotoxin. In dose-response experiments at the same preload, the endotoxic rings had a lower active tension (3.28 +/- 0.28 vs. 6.55 +/- 0.27 x 10(3) dyn/cm) but the same sensitivity. At Lmax, active tension (12.45 +/- 0.48 vs. 5.01 +/- 0.89 x 10(3) dyn/cm in control vessels) and sensitivity (half-maximum effective dose = 0.68 +/- 0.8 x 10(-6) vs. 1.39 +/- 0.29 x 10(-6) M in control vessels) were greater for endotoxic rings. These experiments show that phenylephrine sensitivity and active tension in the rat femoral artery are increased by endotoxin shock, and the importance of muscle length is implied.

scholarly journals The load dependence and the force-velocity relation in intact myosin filaments from skeletal and smooth muscles

2020 ◽  
Vol 318 (1) ◽  
pp. C103-C110 ◽  
Author(s):  
Yu-Shu Cheng ◽  
Felipe de Souza Leite ◽  
Dilson E. Rassier
Keyword(s):  
Smooth Muscle ◽  
Actin Filaments ◽  
Smooth Muscles ◽  
Load Dependence ◽  
Myosin Filaments ◽  
Velocity Relation ◽  
Force Velocity ◽  
Length Changes ◽  
Muscle Myosin ◽  
First Time

In the present study we evaluated the load dependence of force produced by isolated muscle myosin filaments interacting with fluorescently labeled actin filaments, using for the first time whole native myosin filaments. We used a newly developed approach that allowed the use of physiological levels of ATP. Single filaments composed of either skeletal or smooth muscle myosin and single filaments of actin were attached between pairs of nano-fabricated cantilevers of known stiffness. The filaments were brought into contact to produce force, which caused sliding of the actin filaments over the myosin filaments. We applied load to the system by either pushing or pulling the filaments during interactions and observed that increasing the load increased the force produced by myosin and decreasing the load decreased the force. We also performed additional experiments in which we clamped the filaments at predetermined levels of force, which caused the filaments to slide to adjust the different loads, allowing us to measure the velocity of length changes to construct a force-velocity relation. Force values were in the range observed previously with myosin filaments and molecules. The force-velocity curves for skeletal and smooth muscle myosins resembled the relations observed for muscle fibers. The technique can be used to investigate many issues of interest and debate in the field of muscle biophysics.

scholarly journals Plasticity in canine airway smooth muscle.

1995 ◽  
Vol 105 (1) ◽  
pp. 73-94 ◽  
Author(s):  
V R Pratusevich ◽  
C Y Seow ◽  
L E Ford
Keyword(s):  
Smooth Muscle ◽  
Isometric Force ◽  
Strong Dependence ◽  
Smooth Muscles ◽  
Muscle Length ◽  
Relative Length ◽  
Length Range ◽  
Steady Level ◽  
In Series ◽  
Length Changes

The large volume changes of some hollow viscera require a greater length range for the smooth muscle of their walls than can be accommodated by a fixed array of sliding filaments. A possible explanation is that smooth muscles adapt to length changes by forming variable numbers of contractile units in series. To test for such plasticity we examined the muscle length dependence of shortening velocity and compliance, both of which will vary directly with the number of thick filaments in series. Dog tracheal smooth muscle was studied because its cells are arrayed in long, straight, parallel bundles that span the length of the preparation. In experiments where muscle length was changed, both compliance and velocity showed a strong dependence on muscle length, varying by 1.7-fold and 2.2-fold, respectively, over a threefold range of length. The variation in isometric force was substantially less, ranging from a 1.2- to 1.3-fold in two series of experiments where length was varied by twofold to an insignificant 4% variation in a third series where a threefold length range was studied. Tetanic force was below its steady level after both stretches and releases, and increased to a steady level with 5-6 tetani at 5 min intervals. These results suggest strongly that the number of contractile units in series varies directly with the adapted muscle length. Temporary force depression after a length change would occur if the change transiently moved the filaments from their optimum overlap. The relative length independence of the adapted force is explained by the reforming of the filament lattice to produce optimum force development, with commensurate changes of velocity and compliance.

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