Transient length-related mechanical states in smooth muscle

1994 ◽  
Vol 72 (11) ◽  
pp. 1325-1333 ◽  
Author(s):  
Richard A. Meiss
Keyword(s):  
Mechanical Properties ◽  
Mathematical Model ◽  
Smooth Muscle ◽  
Internal Resistance ◽  
Steady Increase ◽  
Kinetic Properties ◽  
Shortening Velocity ◽  
Force Velocity ◽  
Isotonic Contractions ◽  
Isotonic Shortening

The isotonic shortening of electrically stimulated ovarian ligament smooth muscle strips from rabbits was studied by briefly applying sudden increases in afterload (force steps, 0.6 to 3.0 s long) just sufficient to halt the shortening. Upon removal of the extra afterload, the isotonic shortening velocity significantly increased compared with prestep velocities measured at the same muscle lengths. The degree of potentiation depended upon the duration of the force step. Muscles yielded initially when the step was applied, and their stiffness decreased. During the zero-velocity portion of the force step there was a steady increase in stiffness back to levels appropriate to that force. Complete force–velocity curves were made following short (0.6 s) and long (3.0 s) force steps. The values for Vmax (and all intermediate velocities) were significantly greater following a long force step. In a final experimental series, muscles were held isometric immediately after removal of the force step. Force rose monotonically, with a more rapid redevelopment following a long force step. A mathematical model is presented, according to which the effect of the duration of the force step on the poststep mechanical properties may be due to either the alteration of an internal resistance to shortening or a change in the kinetic properties of the cross-bridge array. A hypothesis is proposed relating the steady decline in isotonic shortening velocity to a partial local depletion of energy-yielding substrates.Key words: smooth muscle, isotonic contractions, mechanics, models.

Mechanical properties of pulmonary arteries from sensitized dogs

1983 ◽  
Vol 55 (6) ◽  
pp. 1669-1673 ◽  
Author(s):  
S. K. Kong ◽  
N. L. Stephens
Keyword(s):  
Mechanical Properties ◽  
Pulmonary Arteries ◽  
Maximal Velocity ◽  
Shortening Velocity ◽  
Littermate Control ◽  
Velocity Of Shortening ◽  
Force Velocity ◽  
Tetanic Tension ◽  
Isotonic Shortening

On the basis of isometric dose-response studies, we (J. Pharmacol. Exp. Ther. 219:551-557, 1981) have reported that the ovalbumin-sensitized (S) canine pulmonary artery (PA) is hypersensitive and hyperractive to histamine compared with that from a littermate control (C) in vitro. In this study, our aim was to determine whether the maximal velocity of shortening (Vmax) measured in strips of electrically stimulated SPA and CPA differed. Vmax (velocity at zero load) was obtained by analysis of force-velocity curves from these tissues using the equation (P + a) (V + b) = (Po + a)b, in which P is load, Po is maximum tetanic tension, V is shortening velocity, and a and b are asymptotic values in units of force and velocity. The Vmax values derived for SPA and CPA are 0.188 +/- 0.029 (SE) and 0.113 + 0.017 lo/s, respectively, lo being defined as that length at which Po is obtained. This result indicated that the Vmax value of SPA is significantly (P less than 0.05) different from that of CPA. The b values for SPA [0.034 +/- 0.003 lo/s] and for CPA [0.025 +/- 0.004 lo/s] were also significantly different. However, the force constants a and Po were unchanged in the SPA and CPA. SPA also had a greater isotonic shortening capacity than CPA. These findings indicate that mechanical properties of SPA are altered and lend an understanding of the hyperreactivity of these vessels in the sensitized model.

Contraction history modulates isotonic shortening velocity in smooth muscle

1993 ◽  
Vol 265 (2) ◽  
pp. C467-C476 ◽  
Author(s):  
S. J. Gunst ◽  
M. F. Wu ◽  
D. D. Smith
Keyword(s):  
Smooth Muscle ◽  
Muscle Length ◽  
Electrical Field Stimulation ◽  
Contractile Element ◽  
Shortening Velocity ◽  
Linear Rate ◽  
Velocity Relationship ◽  
Force Velocity ◽  
Contractile Activation ◽  
Isotonic Shortening

The effect of contraction history on the isotonic shortening velocity of canine tracheal smooth muscle was investigated. Muscles were contracted isometrically for 20 s at initial lengths of L(o) (length of maximal active force), 85% L(o), or 70% L(o) using electrical field stimulation. Muscles were then allowed to shorten isotonically under different afterloads either with or without first being subjected to a step decrease in length to 70% L(o). Instantaneous velocities were plotted against instantaneous muscle length during isotonic shortening. Regardless of protocol, the velocity at any muscle length during shortening was lower when the muscle was initially activated at a longer length. The isotonic shortening velocity decreased progressively during shortening at a nearly linear rate with respect to instantaneous muscle length under all conditions. Results suggest that a longer muscle length at the time of activation leads to the development of higher loads on the contractile element during subsequent shortening, resulting in a slower shortening velocity. This plasticity of the force-velocity relationship may result from cytostructural reorganization of the smooth muscle cells in response to contractile activation at different muscle lengths.

Maximum shortening velocity of smooth muscle: zero load-clamp vs. afterloaded method

1983 ◽  
Vol 55 (5) ◽  
pp. 1630-1633 ◽  
Author(s):  
R. W. Mitchell ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Direct Measurement ◽  
Hill Equation ◽  
Shortening Velocity ◽  
Optimal Length ◽  
Lever System ◽  
Technical Advances ◽  
Force Velocity ◽  
The Hill ◽  
Isotonic Shortening

Previous reports from this laboratory of force-velocity relationships of canine tracheal smooth muscle (TSM) have presented maximum shortening velocities (Vmax) mathematically derived from the linearized transformation of the Hill equation (A. V. Hill, Proc. Roy. Soc. London, Ser. B., 126:136-195, 1938). Recent technical advances enable us to measure Vmax directly using an electromagnetic lever system that can instantaneously clamp to a zero load, thus we compared values of Vmax derived mathematically and those directly measured on the same TSM strips. Derived Vmax values from afterloaded isotonic shortening curves for loads greater than preload were 0.328 +/- 0.021 optimal length (lO)/s and were not significantly different from zero load-clamp measurements of 0.301 +/- 0.022 lO/s from the same (n = 15) muscles. These data indicate that Vmax values mathematically derived for TSM from conventional isotonic afterloaded force-velocity curves are valid estimates of zero load velocity, because they were not significantly different from values obtained by direct measurement using the zero load-clamp technique.

Different ontogeny of rate of force generation and shortening velocity in guinea pig trachealis

2000 ◽  
Vol 88 (4) ◽  
pp. 1338-1345 ◽  
Author(s):  
Pasquale Chitano ◽  
Jizhong Wang ◽  
Carrie M. Cox ◽  
Newman L. Stephens ◽  
Thomas M. Murphy
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Force Production ◽  
Internal Resistance ◽  
Force Generation ◽  
Stress Generation ◽  
Shortening Velocity ◽  
Smooth Muscle Function ◽  
Old Adult ◽  
Force Velocity

Juveniles of many species, including humans, display greater airway responsiveness than do adults. This may involve changes in airway smooth muscle function. In the present work we studied force production and shortening velocity in trachealis from 1-wk-old (1 wk), 3-wk-old (3 wk), and 3-mo-old (adult) guinea pigs. Strips were electrically stimulated (60 Hz, 18 V) at their optimal length ( l o) to obtain maximum active stress (Po) and rate of stress generation. Then, force-velocity curves were elicited at 2.5 s from the onset of the stimulus. By applying a recently developed modification of Hill's equation for airway smooth muscle, the maximum shortening velocity at zero load ( V o) and the value α ⋅ γ/β, an index of internal resistance to shortening (Rsi), were calculated (α, β, and γ are the constants of the equation). Poincreased little with maturation, whereas the rate of stress generation increased significantly (0.40 ± 0.03, 0.45 ± 0.03, 0.51 ± 0.03 P o/s for 1 wk, 3 wk, and adult animals). V o slightly increased early with maturation to decrease significantly later (1.79 ± 0.67, 2.45 ± 0.92, and 0.55 ± 0.09 l o/s for 1 wk, 3 wk, and adult animals), whereas the Rsi showed an opposite trend (14.98 ± 5.19, 8.99 ± 3.01, and 32.07 ± 5.54 mN ⋅ mm−2 ⋅ l o −1 ⋅ s for 1 wk, 3 wk, and adult animals). This early increase of force generation in combination with late increase of Rsi may explain the changes of V o with age. An elevated V o may contribute to the incidence of airway hyperresponsiveness in healthy juveniles.

Mechanics of K(+)-induced isotonic and isometric contractions in isolated canine coronary microarteries

1990 ◽  
Vol 258 (3) ◽  
pp. C512-C523 ◽  
Author(s):  
P. J. Boels ◽  
V. A. Claes ◽  
D. L. Brutsaert
Keyword(s):  
Smooth Muscle ◽  
Contractile Activity ◽  
Smooth Muscle Contraction ◽  
Isometric Contractions ◽  
Maximal Velocity ◽  
Physiological Control ◽  
Force Relation ◽  
Force Velocity ◽  
Isotonic Contractions ◽  
Isotonic Shortening

The effects of shortening in isotonic contractions on the mechanics of microvascular smooth muscle were investigated. Intramyocardial canine coronary microarteries (in situ diameter 60 +/- 3 microns) were mounted as rings, connected to a newly developed photoelectromagnetic force-length transducer, and activated with 125 mM K+. Shortening during isotonic contractions depressed the length-force relation (shortening deactivation) compared with the length-force relation obtained from isometric contractions; the effect was present at the earliest moments after activation, suggesting that a fundamental mechanism associated with the actual sliding of contractile filaments delayed onset of contractile activity in isotonic contractions compared with isometric contractions. Force-velocity relations were obtained by isotonic quick releases from isotonic and isometric contractions at various times. Isotonic shortening before the quick releases reduced the constants of the apparent hyperbolic force-velocity relations and maximal velocity of shortening (Vmax) compared with isometric contractions released at the same time. Increasing contraction duration reduced Vmax but more so in isotonic than in isometric contractions. Vmax also decreased with decreasing instantaneous length. A possible effect of force development on Vmax before the isotonic quick release was also described. Quick increments of load during isotonic contractions were sustained during active shortening in the phasic part, but during the tonic part loading resulted in a pronounced transient relaxation. Thus, in microvascular preparations, active isotonic shortening altered the length-force, force-velocity, and velocity-time relations and uncovered a time-dependent sensitivity to loading conditions. These experiments suggested that the mechanics of smooth muscle contraction may contribute significantly to the mechanisms of the physiological control of coronary microvascular diameter.

Myosin phosphorylation and contraction of feline esophageal smooth muscle

1985 ◽  
Vol 249 (1) ◽  
pp. C9-C14 ◽  
Author(s):  
N. W. Weisbrodt ◽  
R. A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Mechanical Activation ◽  
Smooth Muscles ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Muscle Layer ◽  
Field Stimulation ◽  
Shortening Velocity ◽  
Myosin Phosphorylation ◽  
Isotonic Shortening

We tested the hypothesis that phosphorylation of the 20,000-Da light chain of myosin (LC 20) is related to mechanical activation of esophageal smooth muscle. Circular muscle layer strips of cat esophagus were taken from the lower esophageal sphincter (LES) and the distal esophageal body (EB). The LES strips developed tone spontaneously, and the EB strips were tonically contracted with carbachol. Both tissues relaxed in response to electrical-field stimulation. Phosphorylation of the LC 20 was determined in tissues quick-frozen during relaxation and during stress redevelopment after cessation of field stimulation. Stress and phosphorylation levels were low after 30 s of field stimulation, and a rapid contraction followed field stimulation. Phosphorylation in the LES increased from 0.043 +/- 0.029 to 0.328 +/- 0.043 mol Pi/mol LC 20 within 10 s after stimulation of the inhibitory nerves was terminated, while stress was still rising rapidly. Phosphorylation in the LES then declined to a steady-state value of 0.162 +/- 0.034 mol Pi/mol LC 20 after 10 min. Isotonic shortening velocities at a constant afterload following a quick release showed changes with time that were proportional to the level of phosphorylation. This was also true for values of maximal shortening velocity estimated for zero external load and for the rate of stress redevelopment after a step shortening. Comparable measurements were made in the carbachol-contracted EB. These results indicate that visceral smooth muscles, which normally function tonically (LES) or phasically (EB), exhibit an initial rapid mechanical activation associated with myosin phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of microtubule disruption on force, velocity, stiffness and [Ca2+]i in porcine coronary arteries

2000 ◽  
Vol 279 (5) ◽  
pp. H2493-H2501 ◽  
Author(s):  
Richard J. Paul ◽  
Peggy Sue Bowman ◽  
Michael S. Kolodney
Keyword(s):  
Smooth Muscle ◽  
Coronary Arteries ◽  
Isometric Force ◽  
Shortening Velocity ◽  
Cultured Fibroblasts ◽  
Microtubule Disruption ◽  
Highly Sensitive ◽  
Artery Stiffness ◽  
Force Velocity ◽  
Microtubule Stabilizer

Force generated by smooth muscle cells is believed to result from the interaction of actin and myosin filaments and is regulated through phosphorylation of the myosin regulatory light chain (LC20). The role of other cytoskeleton filaments, such as microtubules and intermediate filaments, in determining the mechanical output of smooth muscle is unclear. In cultured fibroblasts, microtubule disruption results in large increases in force similar to contractions associated with LC20 phosphorylation (15). One hypothesis, the “tensegrity” or “push-pull” model, attributes this increase in force to the disruption of microtubules functioning as rigid struts to resist force generated by actin-myosin interaction (9). In porcine coronary arteries, the disruption of microtubules by nocodazole (11 μM) also elicited moderate but significant increases in isometric force (10–40% of a KCl contracture), which could be blocked or reversed by taxol (a microtubule stabilizer). We tested whether this nocodazole-induced force was accompanied by changes in coronary artery stiffness or unloaded shortening velocity, parameters likely to be highly sensitive to microtubule resistance elements. Few changes were seen, ruling out push-pull mechanisms for the increase in force by nocodazole. In contrast, the intracellular calcium concentration, measured by fura 2 in the intact artery, was increased by nocodazole in parallel with force, and this was inhibited and/or reversed by taxol. Our results indicate that microtubules do not significantly contribute to vascular smooth muscle mechanical characteristics but, importantly, may play a role in modulation of Ca2+ signal transduction.

Effect of airway inflammation on smooth muscle shortening and contractility in guinea pig trachealis

1993 ◽  
Vol 265 (6) ◽  
pp. L549-L554 ◽  
Author(s):  
R. W. Mitchell ◽  
I. M. Ndukwu ◽  
K. Arbetter ◽  
J. Solway ◽  
A. R. Leff
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Neurogenic Inflammation ◽  
Isometric Force ◽  
Electrical Field Stimulation ◽  
Shortening Velocity ◽  
Lever System ◽  
Force Velocity

We studied the effect of either 1) immunogenic inflammation caused by aerosolized ovalbumin or 2) neurogenic inflammation caused by aerosolized capsaicin in vivo on guinea pig tracheal smooth muscle (TSM) contractility in vitro. Force-velocity relationships were determined for nine epithelium-intact TSM strips from ovalbumin-sensitized (OAS) vs. seven sham-sensitized controls and TSM strips for seven animals treated with capsaicin aerosol (Cap-Aer) vs. eight sham controls. Muscle strips were tethered to an electromagnetic lever system, which allowed isotonic shortening when load clamps [from 0 to maximal isometric force (Po)] were applied at specific times after onset of contraction. Contractions were elicited by supramaximal electrical field stimulation (60 Hz, 10-s duration, 18 V). Optimal length for each muscle was determined during equilibration. Maximal shortening velocity (Vmax) was increased in TSM from OAS (1.72 +/- 0.46 mm/s) compared with sham-sensitized animals (0.90 +/- 0.15 mm/s, P < 0.05); Vmax for TSM from Cap-Aer (0.88 +/- 0.11 mm/s) was not different from control TSM (1.13 +/- 0.08 mm/s, P = NS). Similarly, maximal shortening (delta max) was augmented in TSM from OAS (1.01 +/- 0.15 mm) compared with sham-sensitized animals (0.72 +/- 0.14 mm, P < 0.05); delta max for TSM from Cap-Aer animals (0.65 +/- 0.11 mm) was not different from saline aerosol controls (0.71 +/- 0.15 mm, P = NS). We demonstrate Vmax and delta max are augmented in TSM after ovalbumin sensitization; in contrast, neurogenic inflammation caused by capsaicin has no effect on isolated TSM contractility in vitro. These data suggest that airway hyperresponsiveness in vivo that occurs in association with immunogenic or neurogenic inflammation may result from different effects of these types of inflammation on airway smooth muscle.

Cross-bridge dephosphorylation and relaxation of vascular smooth muscle

1989 ◽  
Vol 256 (2) ◽  
pp. C282-C287 ◽  
Author(s):  
C. M. Hai ◽  
R. A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Time Course ◽  
Electrical Field Stimulation ◽  
Shortening Velocity ◽  
Electrical Field ◽  
Cross Bridge ◽  
Time Course Data ◽  
Necessary And Sufficient ◽  
Isotonic Shortening

We tested the hypothesis that relaxation in vascular smooth muscle is the result of inactivation of myosin light chain kinase and cross-bridge dephosphorylation. Fast neurally mediated contractions of swine carotid medial strips were induced by electrical field stimulation. Termination of the stimulus resulted in relaxation with a half time of 2 min. Nifedipine (0.1 microM) increased the relaxation rate without significant effects on the contractile response. Cross-bridge dephosphorylation was much faster than stress decay with basal levels reached within 1 min when 73% of the developed stress remained. The time-course data of dephosphorylation and stress were analyzed with a model that predicted the dependences of stress and isotonic shortening velocity on cross-bridge phosphorylation during contraction. Rate constants resolved from contraction data also fitted the relaxation data when the model's prediction was corrected for estimated errors in the phosphorylation measurements. Because Ca2+-dependent cross-bridge phosphorylation was the only postulated regulatory mechanism in the model, these results are consistent with the hypothesis that cross-bridge dephosphorylation is necessary and sufficient to explain relaxation in the swine carotid media.

scholarly journals Slowing of velocity during isotonic shortening in single isolated smooth muscle cells. Evidence for an internal load.

1990 ◽  
Vol 96 (3) ◽  
pp. 581-601 ◽  
Author(s):  
D E Harris ◽  
D M Warshaw
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Isometric Force ◽  
Muscle Cells ◽  
Force Transducer ◽  
Cell Stiffness ◽  
Shortening Velocity ◽  
Internal Load ◽  
Isolated Smooth Muscle Cells ◽  
Isotonic Shortening

In single smooth muscle cells, shortening velocity slows continuously during the course of an isotonic (fixed force) contraction (Warshaw, D.M. 1987. J. Gen. Physiol. 89:771-789). To distinguish among several possible explanations for this slowing, single smooth muscle cells were isolated from the gastric muscularis of the toad (Bufo marinus) and attached to an ultrasensitive force transducer and a length displacement device. Cells were stimulated electrically and produced maximum stress of 144 mN/mm2. Cell force was then reduced to and maintained at preset fractions of maximum, and cell shortening was allowed to occur. Cell stiffness, a measure of relative numbers of attached crossbridges, was measured during isotonic shortening by imposing 50-Hz sinusoidal force oscillations. Continuous slowing of shortening velocity was observed during isotonic shortening at all force levels. This slowing was not related to the time after the onset of stimulation or due to reduced isometric force generating capacity. Stiffness did not change significantly over the course of an isotonic shortening response, suggesting that the observed slowing was not the result of reduced numbers of cycling crossbridges. Furthermore, isotonic shortening velocity was better described as a function of the extent of shortening than as a function of the time after the onset of the release. Therefore, we propose that slowing during isotonic shortening in single isolated smooth muscle cells is the result of an internal load that opposes shortening and increases as cell length decreases.

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