scholarly journals Force: velocity relationship in single isolated toad stomach smooth muscle cells.

1987 ◽  
Vol 89 (5) ◽  
pp. 771-789 ◽  
Author(s):  
D M Warshaw
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Striated Muscle ◽  
Muscle Cells ◽  
Length Change ◽  
Force Transducer ◽  
Cell Length ◽  
Shortening Velocity ◽  
Cross Sectional ◽  
Cross Bridges

The relationship between force and shortening velocity (F:V) in muscle is believed to reflect both the mechanics of the myosin cross-bridge and the kinetics of its interaction with actin. To date, the F:V for smooth muscle cells has been inferred from F:V data obtained in multicellular tissue preparations. Therefore, to determine F:V in an intact single smooth muscle cell, cells were isolated from the toad (Bufo marinus) stomach muscularis and attached to a force transducer and length displacement device. Cells were electrically stimulated at 20 degrees C and generated 143 mN/mm2 of active force per muscle cross-sectional area. At the peak of contraction, cells were subjected to sudden changes in force (dF = 0.10-0.90 Fmax) and then maintained at the new force level. The force change resulted in a length response in which the cell length (Lcell) rapidly decreased during the force step and then decreased monotonically with a time constant between 75 and 600 ms. The initial length change that coincided with the force step was analyzed and an active cellular compliance of 1.9% cell length was estimated. The maintained force and resultant shortening velocity (V) were fitted to the Hill hyperbola with constants a/Fmax of 0.268 and b of 0.163 Lcell/s. Vmax was also determined by a procedure in which the cell length was slackened and the time of unloaded shortening was recorded (slack test). From the slack test, Vmax was estimated as 0.583 Lcell/s, in agreement with the F:V data. The F:V data were analyzed within the framework of the Huxley model (Huxley. 1957. Progress in Biophysics and Biophysical Chemistry. 7:255-318) for contraction and interpreted to indicate that in smooth muscle, as compared with fast striated muscle, there may exist a greater percentage of attached force-generating cross-bridges.

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.

Dense-body aggregates as plastic structures supporting tension in smooth muscle cells

2010 ◽  
Vol 299 (5) ◽  
pp. L631-L638 ◽  
Author(s):  
Jie Zhang ◽  
Ana M. Herrera ◽  
Peter D. Paré ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Striated Muscle ◽  
Dense Body ◽  
Muscle Cells ◽  
Cell Length ◽  
Structural Basis ◽  
Airway Smooth Muscle Cells ◽  
Dense Bodies ◽  
Large Length

The wall of hollow organs of vertebrates is a unique structure able to generate active tension and maintain a nearly constant passive stiffness over a large volume range. These properties are predominantly attributable to the smooth muscle cells that line the organ wall. Although smooth muscle is known to possess plasticity (i.e., the ability to adapt to large changes in cell length through structural remodeling of contractile apparatus and cytoskeleton), the detailed structural basis for the plasticity is largely unknown. Dense bodies, one of the most prominent structures in smooth muscle cells, have been regarded as the anchoring sites for actin filaments, similar to the Z-disks in striated muscle. Here, we show that the dense bodies and intermediate filaments formed cable-like structures inside airway smooth muscle cells and were able to adjust the cable length according to cell length and tension. Stretching the muscle cell bundle in the relaxed state caused the cables to straighten, indicating that these intracellular structures were connected to the extracellular matrix and could support passive tension. These plastic structures may be responsible for the ability of smooth muscle to maintain a nearly constant tensile stiffness over a large length range. The finding suggests that the structural plasticity of hollow organs may originate from the dense-body cables within the smooth muscle cells.

A method for isolating adult and neonatal airway smooth muscle cells and measuring shortening velocity

1999 ◽  
Vol 86 (1) ◽  
pp. 427-435 ◽  
Author(s):  
S. P. Driska ◽  
R. E. Laudadio ◽  
M. R. Wolfson ◽  
T. H. Shaffer
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Single Cell ◽  
Airway Smooth Muscle ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Cell Length ◽  
Airway Smooth Muscle Cells ◽  
Shortening Velocity ◽  
Adult Cells

Methods are described for isolating smooth muscle cells from the tracheae of adult and neonatal sheep and measuring the single-cell shortening velocity. Isolated cells were elongated, Ca2+ tolerant, and contracted rapidly and substantially when exposed to cholinergic agonists, KCl, serotonin, or caffeine. Adult cells were longer and wider than preterm cells. Mean cell length in 1.6 mM CaCl2 was 194 ± 57 (SD) μm ( n = 66) for adult cells and 93 ± 32 μm ( n = 20) for preterm cells ( P < 0.05). Mean cell width at the widest point of the adult cells was 8.2 ± 1.8 μm ( n = 66) and 5.2 ± 1.5 μm ( n = 20) for preterm cells ( P < 0.05). Cells were loaded into a perfusion dish maintained at 35°C and exposed to agonists, and contractions were videotaped. Cell lengths were measured from 30 video frames and plotted as a function of time. Nonlinear fitting of cell length to an exponential model gave shortening velocities faster than most of those reported for airway smooth muscle tissues. For a sample of 10 adult and 10 preterm cells stimulated with 100 μM carbachol, mean (± SD) shortening velocity of the preterm cells was not different from that of the adult cells (0.64 ± 0.30 vs. 0.54 ± 0.27 s−1, respectively), but preterm cells shortened more than adult cells (68 ± 12 vs. 55 ± 11% of starting length, respectively; P < 0.05). The preparative and analytic methods described here are widely applicable to other smooth muscles and will allow contraction to be studied quantitatively at the single-cell level.

Structure-function correlation in airway smooth muscle adapted to different lengths

2003 ◽  
Vol 285 (2) ◽  
pp. C384-C390 ◽  
Author(s):  
Kuo-Hsing Kuo ◽  
Ana M. Herrera ◽  
Lu Wang ◽  
Peter D. Paré ◽  
Lincoln E. Ford ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Power ◽  
Isometric Force ◽  
Muscle Length ◽  
Length Change ◽  
Cell Length ◽  
Myosin Filament ◽  
Shortening Velocity ◽  
Cross Sectional

Airway smooth muscle is able to adapt and maintain a nearly constant maximal force generation over a large length range. This implies that a fixed filament lattice such as that found in striated muscle may not exist in this tissue and that plastic remodeling of its contractile and cytoskeletal filaments may be involved in the process of length adaptation that optimizes contractile filament overlap. Here, we show that isometric force produced by airway smooth muscle is independent of muscle length over a twofold length change; cell cross-sectional area was inversely proportional to cell length, implying that the cell volume was conserved at different lengths; shortening velocity and myosin filament density varied similarly to length change: increased by 69.4% ± 5.7 (SE) and 76.0% ± 9.8, respectively, for a 100% increase in cell length. Muscle power output, ATPase rate, and myosin filament density also have the same dependence on muscle cell length: increased by 35.4% ± 6.7, 34.6% ± 3.4, and 35.6% ± 10.6, respectively, for a 50% increase in cell length. The data can be explained by a model in which additional contractile units containing myosin filaments are formed and placed in series with existing contractile units when the muscle is adapted at a longer length.

scholarly journals Expression of smooth muscle myosin heavy chains and unloaded shortening in single smooth muscle cells

1997 ◽  
Vol 273 (4) ◽  
pp. C1259-C1266 ◽  
Author(s):  
Daniel P. Meer ◽  
Thomas J. Eddinger
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Polymerase Chain Reaction Amplification ◽  
Mrna Level ◽  
Muscle Cells ◽  
Smooth Muscle Myosin ◽  
Minimum Length ◽  
Shortening Velocity ◽  
Variable Expression ◽  
Muscle Myosin

The functional significance of the variable expression of the smooth muscle myosin heavy chain (SM-MHC) tail isoforms, SM1 and SM2, was examined at the mRNA level (which correlates with the protein level) in individual permeabilized rabbit arterial smooth muscle cells (SMCs). The length of untethered single permeabilized SMCs was monitored during unloaded shortening in response to increased Ca2+ (pCa 6.0), histamine (1 μM), and phenylephrine (1 μM). Subsequent to contraction, the relative expression of SM1 and SM2 mRNAs from the same individual SMCs was determined by reverse transcription-polymerase chain reaction amplification and densitometric analysis. Correlational analyses between the SM2-to-SM1 ratio and unloaded shortening in saponin- and α-toxin-permeabilized SMCs ( n = 28) reveal no significant relationship between the SM-MHC tail isoform ratio and unloaded shortening velocity. The best correlations between SM2/SM1 and the contraction characteristics of untethered vascular SMCs were with the minimum length attained following contraction ( n = 20 and r = 0.72 for α-toxin, n = 8 and r = 0.78 for saponin). These results suggest that the primary effect of variable expression of the SM1 and SM2 SM-MHC tail isoforms is on the cell final length and not on shortening velocity.

Agonist activation modulates cross-bridge states in single vascular smooth muscle cells

1993 ◽  
Vol 264 (1) ◽  
pp. C103-C108 ◽  
Author(s):  
F. V. Brozovich ◽  
M. Yamakawa
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Relative Population ◽  
Cross Bridge ◽  
Cross Bridges ◽  
State Force

To determine cross-bridge properties during agonist-stimulated contractions, steady-state force and relative steady-state stiffness were recorded at rest (pCa 9) and during both full (pCa 4) and partial (pCa 7) Ca2+ activations of isolated single alpha-toxin permeabilized vascular smooth muscle cells. For pCa 4 and pCa 7, agonist (1 microM histamine) activation resulted in significant (P < 0.05) increases in both force and stiffness. The agonist-induced increase of steady-state force was significantly (P < 0.05) greater than that of stiffness; at pCa 4, there was a 48% increase for force vs. 17% for stiffness, and, at pCa 7, there was a 160% increase for force vs. 57% for stiffness. The increase in force and stiffness after agonist prestimulation implies that the number of attached cross bridges has increased. However, after agonist prestimulation, we found that the increase of force was greater (P < 0.05) than that of stiffness, resulting in a greater force at any given level of stiffness. Thus these data indicate that agonist activation, presumably via activation of a G protein, increases the relative force per attached cross bridge, possibly by modulating the kinetics of the actomyosin adenosinetriphosphatase to increase in the relative population of cross bridges in force-producing states [actinomyosin (AM) or AM.ADP].

scholarly journals Comparison of pain intensity, smooth muscle cells density, and alpha-smooth muscle actin expression in ovarial and peritoneal endometriosis

2021 ◽  
Vol 29 (3) ◽  
pp. 108
Author(s):  
Sutrisno Sutrisno ◽  
Muhammad Nooryanto ◽  
Shella Widya Gani
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Pain Intensity ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Alpha Smooth Muscle Actin ◽  
Cross Sectional ◽  
Muscle Density ◽  
Peritoneal Endometriosis

HIGHLIGHT1. Pain intensity, smooth muscle cells density, and alpha-SMA expression can be used to analyze the role of smooth muscle in endometriosis.2. Compared to healthy individuals, those with endometriosis have higher pain intensity, smooth muscle cells density, and alpha-SMA expression. 3. Among endometriotic patients, those with peritoneal endometriosis have higher pain intensity, smooth muscle cells density, and alpha-SMA expression than those with ovarial endometriosis.3. The expression of alpha-SMA, smooth muscle density, and pain intensity were found to correlate significantly in endometriosis. ABSTRACTObjectives: to identify the role of smooth muscle through the analysis of smooth muscle cells density, expression of a-SMA, and the pain intensity.Materials and Methods: Study design is a cross sectional analytic observational. Study sample consists of women with ovarial endometrios and women with peritoneal endometriosis that undergo laparoscopy and laparotomy in RSUD Saiful Anwar Malang and RSIA Melati Malang from January until December 2019. There are 16 samples: 8 samples of ovarial endometriosis and 8 samples of peritoneal endometriosis. Smooth muscle cell density was analyzed by comparing the number of smooth muscle cells with the total area of endometriosis tissue in one microscopical field. a-SMA expression obtained by immunohistochemistry. Degree of pain obatined by filling the part 1 point 1-11 of EHP-30 queistionnaire the day after the procedure. Data was analyzed by Independent T-test and Pearson correlation.Results: Pain intensity, smooth muscle cells density, and a-SMA expression is higher in the endometriosis patient compared to healthy individual. Pain intensity, smooth muscle cells density, and a-SMA expression is lower in the ovarial endometriosis compared to peritoneal endometriosis.Conclusion: There are a significant correlation between the expression of a-SMA, smooth muscle density, and pain intensity in endometriosis.

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