Mechanical properties of tracheal smooth muscle: effects of temperature

1977 ◽  
Vol 233 (3) ◽  
pp. C92-C98 ◽  
Author(s):  
N. L. Stephens ◽  
R. Cardinal ◽  
B. Simmons
Keyword(s):  
Smooth Muscle ◽  
Tracheal Smooth Muscle ◽  
Effect Of Temperature ◽  
Contractile Element ◽  
Tension Development ◽  
In Series ◽  
Force Velocity ◽  
Effects Of Temperature ◽  
Active Processes ◽  
The Hill

The effect of temperature on the isometric tetanic myogram was studied in isolated canine tracheal smooth muscle (TSM). At 37 degrees C and 27 degrees C no significant change occurred in maximum tetanic tension (PO). At 17 degrees C a significant reduction was seen Values of Q10 for contraction time (tPO) were almost halved, whereas those for rate of tension development (dP/dt) were almost doubled. The effect of the same temperatures on the force-velocity (F-v) relationships was also studied. All three F-v curves were described by the Hill equation, (P + a) (v + b) = (PO + a)b. Vmax and b decreased with decreased temperature, with Q10's demonstrating they were dependent on active processes. Finally, the decreased dP/dt of the myogram at lower temperatures was felt to be the probable result of decreased contractile element velocity because no decrease in series elastic component stiffness was demonstrable, there being instead an increase in stiffness at lower temperatures.

Effects of active shortening on tension development of rabbit papillary muscle

1980 ◽  
Vol 238 (1) ◽  
pp. H8-H13 ◽  
Author(s):  
J. K. Leach ◽  
A. J. Brady ◽  
B. J. Skipper ◽  
D. L. Millis
Keyword(s):  
Isometric Tension ◽  
Isometric Contractions ◽  
Tension Development ◽  
Velocity Of Shortening ◽  
Tension Time ◽  
Shortening Deactivation ◽  
Force Velocity ◽  
Stimulus Length ◽  
The Right ◽  
The Hill

Duration and intensity of force development have been shown to be less during active muscle shortening than during isometric contraction. The purpose of this study was to compare force developed during controlled shortening with that predicted by the Frank-Starling relation. Paillary muscles from the right ventricles of rabbits were arranged for isometric tension recording, and isometric contractions were recorded at several lengths. The muscles were then permitted to shorten at velocities of 0.2--6 mm/s, shortening beginning 150--200 ms after the stimulus. Length-tension-time curves constructed from the isometric contractions were used to determine predicted shortening tension (Pp), which was compared with actual tension during shortening (Ps) at corresponding times and lengths. Ps was significantly less than Pp and the ratio Ps/Pp decreased with increasing velocity of shortening. The decrease in Ps/Pp was directly related to the duration of shortening (P less than 0.001), suggesting that the fall of shortening tension reflected both the Hill force-velocity relation and shortening deactivation.

Tension development during contractile stimulation of smooth muscle requires recruitment of paxillin and vinculin to the membrane

2004 ◽  
Vol 286 (2) ◽  
pp. C433-C447 ◽  
Author(s):  
Anabelle Opazo Saez ◽  
Wenwu Zhang ◽  
Yidi Wu ◽  
Christopher E. Turner ◽  
Dale D. Tang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Focal Adhesions ◽  
Smooth Muscle Contraction ◽  
Cytoskeletal Proteins ◽  
Tracheal Smooth Muscle ◽  
Muscle Membrane ◽  
Tension Development ◽  
Muscle Tissues ◽  
Primary Determinant ◽  
Smooth Muscle Membrane

Cytoskeletal reorganization of the smooth muscle cell in response to contractile stimulation may be an important fundamental process in regulation of tension development. We used confocal microscopy to analyze the effects of cholinergic stimulation on localization of the cytoskeletal proteins vinculin, paxillin, talin and focal adhesion kinase (FAK) in freshly dissociated tracheal smooth muscle cells. All four proteins were localized at the membrane and throughout the cytoplasm of unstimulated cells, but their concentration at the membrane was greater in acetylcholine (ACh)-stimulated cells. Antisense oligonucleotides were introduced into tracheal smooth muscle tissues to deplete paxillin protein, which also inhibited contraction in response to ACh. In cells dissociated from paxillin-depleted muscle tissues, redistribution of vinculin to the membrane in response to ACh was prevented, but redistribution of FAK and talin was not inhibited. Muscle tissues were transfected with plasmids encoding a paxillin mutant containing a deletion of the LIM3 domain (paxillin LIM3 dl 444–494), the primary determinant for targeting paxillin to focal adhesions. Expression of paxillin LIM3 dl in muscle tissues also inhibited contractile force and prevented cellular redistribution of paxillin and vinculin to the membrane in response to ACh, but paxillin LIM3 dl did not inhibit increases in intracellular Ca2+ or myosin light chain phosphorylation. Our results demonstrate that recruitment of paxillin and vinculin to smooth muscle membrane is necessary for tension development and that recruitment of vinculin to the membrane is regulated by paxillin. Vinculin and paxillin may participate in regulating the formation of linkages between the cytoskeleton and integrin proteins that mediate tension transmission between the contractile apparatus and the extracellular matrix during smooth muscle contraction.

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.

Force–velocity relationships in hypertensive arterial smooth muscle

1985 ◽  
Vol 63 (6) ◽  
pp. 669-674 ◽  
Author(s):  
C. S. Packer ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rat ◽  
Peripheral Resistance ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Isometric Tension ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Force Velocity ◽  
Wistar Kyoto

Increased total peripheral resistance is the cardinal haemodynamic disorder in essential hypertension. This could be secondary to alterations in the mechanical properties of vascular smooth muscle. Adequate study has not been made of the force–velocity (F–V) relationship in hypertensive arterial smooth muscle. Increased shortening in arterial smooth muscle would result in greater narrowing of arteries. The objectives of this investigation were to see if there is (i) increased shortening or increased maximum change in muscle length (ΔLmax where L stands for muscle length), (ii) an increased maximum velocity of shortening (Vmax) measured in lo per second where lo is the optimal muscle length for tension development, and (iii) a difference in maximum isometric tension (Po) developed in spontaneously hypertensive rat (SHR; N = 6) compared with normotensive Wistar Kyoto rat (WKY; N = 5) caudal artery strips. An electromagnetic muscle lever was employed in recording force–velocity data. Analysis of these data revealed the following: (a) the SHR mean Po of 6.21 ± 1.01 N/cm2 was not different from the mean WKY Po of 6.97 ± 1.64 N/cm2 (p > 0.05); (b) the SHR preparations showed greater shortening for all loads imposed; (c) the SHR Vmax of 0.016 lo/s was greater than the WKY Vmax of 0.013 lo/s (p < 0.05). This study provides evidence that while hypertensive arterial smooth muscle is not able to produce more force than normotensive arterial smooth muscle, it is capable of faster and greater shortening. The latter could result in increased narrowing of hypertensive arteries and increased blood pressure.

Force responses to constant-velocity shortening of electrically stimulated human muscle-tendon complex

1996 ◽  
Vol 81 (1) ◽  
pp. 384-392 ◽  
Author(s):  
C. S. Cook ◽  
M. J. McDonagh
Keyword(s):  
Isometric Force ◽  
Human Muscle ◽  
Maximal Activation ◽  
First Dorsal Interosseus ◽  
In Series ◽  
Velocity Equation ◽  
Force Velocity ◽  
Activation Force ◽  
The Hill ◽  
Different Levels

Force-velocity curves in human muscle often have unexpectedly high forces at high velocities. If series elasticity is the cause, it should have less effect at lower activation levels and larger shortening amplitudes. The first dorsal interosseus muscle-tendon complex was shortened at different levels of activation and by different amplitudes. Force-velocity curves had high force well maintained at high velocities. With an actuator release of 4.21 mm at 80% of maximal activation, force was > 45% of isometric force (Po) for all actuator velocities > 200 mm/s (1.49 muscle lengths/s). At 30% activation, the force was > 25% of Po at these velocities. The smaller 2.46-mm releases produced higher forces than the 4.21-mm releases at these velocities. At 80% activation, force was > 65% of Po, and at 30% activation, it was > 50% of Po at these velocities. Corrections of these data for elasticity produced classic Hill-type force-velocity curves. A model incorporating the Hill force-velocity equation and a spring in series accounts for the results.

Contractile force of canine tracheal smooth muscle during continuous stretch

1982 ◽  
Vol 52 (3) ◽  
pp. 655-663 ◽  
Author(s):  
S. J. Gunst ◽  
J. A. Russell
Keyword(s):  
Smooth Muscle ◽  
Isometric Contraction ◽  
Muscle Force ◽  
Muscle Length ◽  
Force Transducer ◽  
Contractile Force ◽  
Tracheal Smooth Muscle ◽  
Contractile Element ◽  
Active Force ◽  
Force Curve

Canine tracheal smooth muscle strips were mounted horizontally in a tissue bath between a force transducer and a motor-driven movable steel rod, which was used to change muscle length. Muscle length and force were continuously measured during stretch and simultaneously plotted on an X-Y recorder. Active force during stretch was investigated as follows: an initial length was set with the muscle relaxed, where it was contracted isometrically with acetylcholine. After active force reached a steady state, muscle length was decreased until the total tension was equal to zero. The muscle was then stretched slowly to obtain a continuous length-force curve. Results show that force during stretch increases as the length at which the initial isometric contraction is elicited, is decreased. A possible interpretation is that during tonic muscle contraction, the contractile element is able to shorten very slowly relative to the rate at which the muscle was retracted. Thus, the contractile element length established during isometric contraction would affect the muscle force obtained during subsequent stretch of the muscle.

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