Relaxation of smooth muscle

1994 ◽  
Vol 72 (11) ◽  
pp. 1345-1350 ◽  
Author(s):  
N. L. Stephens ◽  
H. Jiang
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Late Phase ◽  
Contractile Element ◽  
Smooth Muscle Relaxation ◽  
Shortening Velocity ◽  
Cycling Rate ◽  
Cross Bridge ◽  
Cross Bridges ◽  
And Control

We have demonstrated that in dogs antigen sensitization results in alterations of contractile properties. These changes could account for the hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining high airway resistance. We therefore developed an index of isotonic relaxation, t1/2,CE (half time for relaxation that is independent of muscle load and initial contractile element length), for evaluation of the relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle than that in controls, studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by t1/2,CE showed no difference between sensitized and control muscles after 10 s of stimulation (8.38 ± 0.92 vs. 7.78 ± 0.93 s, means ± SE); however, it was prolonged significantly in the sensitized muscle only stimulated for 1 s (12.74 ± 2.5 s, mean ± SE) compared with the control (6.98 ± 1.01 s). During the late phase of isotonic relaxation, both groups showed an unexpected spontaneous increase in zero-load shortening velocity, which is an index of cross-bridge cycling rate. We conclude that (i) both contraction and relaxation properties of early normally cycling cross bridges are altered after sensitization and these changes may account for the hyperresponsiveness observed in asthmatics and (ii) the cross-bridge cycling rate increases spontaneously during isotonic relaxation, probably as a result of reactivation of the contractile mechanism.Key words: smooth muscle relaxation, isotonic relaxation, spontaneous activation in late relaxation, mechanisms for airway hyperresponsiveness, new index of muscle relaxation.

Isotonic relaxation of sensitized bronchial smooth muscle

1992 ◽  
Vol 262 (3) ◽  
pp. L344-L350
Author(s):  
H. Jiang ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Relaxation Time ◽  
Airway Resistance ◽  
Late Phase ◽  
Contractile Element ◽  
Half Time ◽  
Shortening Velocity ◽  
Bronchial Smooth Muscle ◽  
The Mean ◽  
And Control

Although the mechanisms underlying asthma are not clear, we have demonstrated that in dogs antigen sensitization results in alterations of contractile properties, such as greater early maximum shortening velocity and capacity of bronchial smooth muscle. These changes could account for the hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining high airway resistance. This, a relatively less-studied area, requires study. In the current study, we therefore developed an index of isotonic relaxation, T1/2,CE (half-time for relaxation which is independent of muscle load and initial contractile element length) for evaluation of the relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle (SBSM) than that in controls studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by T1/2,CE showed no difference between sensitized and control muscles after 10 s of stimulation (8.38 +/- 0.92 s vs. 7.78 +/- 0.93, means +/- SE); however, it was prolonged significantly in SBSM stimulated only for 1 s (12.74 +/- 2.5 s, mean +/- SE) compared with the control (6.98 +/- 1.01). Unexpectedly, we found that during the late phase of isotonic relaxation, both groups showed spontaneous increase in zero load shortening velocity, which is an index of cross-bridge cycling rate.2

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.

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.

scholarly journals Series-to-parallel transition in the filament lattice of airway smooth muscle

2000 ◽  
Vol 89 (3) ◽  
pp. 869-876 ◽  
Author(s):  
Chun Y. Seow ◽  
Victor R. Pratusevich ◽  
Lincoln E. Ford
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Length ◽  
Thick Filament ◽  
Cycling Rate ◽  
Cross Bridge ◽  
Parallel Change ◽  
Force Velocity ◽  
Cross Bridges ◽  
Trachealis Muscle

Force-velocity curves measured at different times during tetani of sheep trachealis muscle were analyzed to assess whether velocity slowing could be explained by thick-filament lengthening. Such lengthening increases force by placing more cross bridges in parallel on longer filaments and decreases velocity by reducing the number of filaments spanning muscle length. From 2 s after the onset of stimulation, when force had achieved 42% of it final value, to 28 s, when force had been at its tetanic plateau for ∼15 s, velocity decreases were exactly matched by force increases when force was adjusted for changes in activation, as assessed from the maximum power value in the force-velocity curves. A twofold change in velocity could be quantitatively explained by a series-to-parallel change in the filament lattice without any need to postulate a change in cross-bridge cycling rate.

Use of a new index to study relaxation in a vascular model of anaphylactic shock

1993 ◽  
Vol 74 (6) ◽  
pp. 2621-2626 ◽  
Author(s):  
X. Liu ◽  
H. Jiang ◽  
N. L. Stephens
Keyword(s):  
Saphenous Vein ◽  
Anaphylactic Shock ◽  
Muscle Activation ◽  
Muscle Relaxation ◽  
Contractile Element ◽  
Time Index ◽  
Muscle Shortening ◽  
Cross Bridges ◽  
And Control ◽  
Relaxation Index

We have reported increased smooth muscle shortening ability in ragweed pollen-sensitized saphenous vein (SSV). This may account for the vascular hyperreactivity of anaphylactic shock. We have now investigated relaxation in SSV. Because isotonic relaxation is load and initial contractile element length dependent, we developed an adjusted half-relaxation time index, which was independent of these variables. Muscle activation state was monitored by measuring maximum unloaded velocity. The relaxation index showed no difference between SSV and control saphenous vein after 2.5, 10, and 15 s of electrical stimulation; however, after 1 s of stimulation it was prolonged significantly in SSV. We concluded that the cross bridges activating early in contraction demonstrated prolonged relaxation. Activation state during muscle relaxation spontaneously increased toward the end of relaxation, coincident with a slowing in isotonic re-elongation rate. This was seen only in muscles relaxing from 15 s of stimulation. Our results indicate that 1) the relaxation properties of early cycling (1 s) cross bridges are altered after sensitization; and 2) toward the end of isotonic relaxation, cross-bridge cycling rate increases spontaneously, a phenomenon not previously reported. We speculate that the rapid re-elongation in late relaxation may reactivate muscle.

cGMP mediates corpus cavernosum smooth muscle relaxation with altered cross-bridge function

Life Sciences ◽  
1998 ◽  
Vol 63 (3) ◽  
pp. 185-194 ◽  
Author(s):  
Alex T. Chuang ◽  
John D. Strauss ◽  
William D. Steers ◽  
Richard A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Corpus Cavernosum ◽  
Smooth Muscle Relaxation ◽  
Bridge Function ◽  
Cross Bridge

Myosin phosphorylation and regulation of cross-bridge cycle in tracheal smooth muscle

1983 ◽  
Vol 244 (3) ◽  
pp. C182-C187 ◽  
Author(s):  
W. T. Gerthoffer ◽  
R. A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Tracheal Smooth Muscle ◽  
Shortening Velocity ◽  
Active Stress ◽  
Myosin Phosphorylation ◽  
Cross Bridge ◽  
Rapid Changes ◽  
Cross Bridges ◽  
Resting Muscle ◽  
Isotonic Shortening

We have tested the hypothesis that phosphorylation of the 20,000-dalton myosin light chains (LC 20) in rabbit tracheal smooth muscle modulates cross-bridge kinetics and isotonic shortening velocity. The thin muscle [190 +/- 10 (SE) microns] allowed detection of rapid changes in carbachol-induced active stress development, LC 20 phosphorylation, and isotonic shortening velocities. Phosphorylation of the LC 20 in resting muscle was 0.12 +/- 0.04 mol Pi/mol LC 20. Carbachol (10(-5) M) increased the level of phosphorylation to 0.46 +/- 0.03 mol Pi/mol LC 20 within 30 s. Phosphorylation then declined significantly as steady-state active stress was reached. A positive correlation was always found between LC 20 phosphorylation and shortening velocity. This result supports the hypothesis that the level of myosin phosphorylation was related to the mean cross-bridge cycling rate rather than the number of cross bridges contributing to the developed stress. Dephosphorylation of LC 20 occurred at about the same rate as the decline in shortening velocity and stress upon stimulus washout.

Relaxation, [Ca2+]i, and the latch-bridge hypothesis in swine arterial smooth muscle

1991 ◽  
Vol 261 (1) ◽  
pp. C41-C50 ◽  
Author(s):  
C. M. Rembold
Keyword(s):  
Smooth Muscle ◽  
Time Course ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Channel Blockers ◽  
Rate Limiting Step ◽  
Bridge Model ◽  
Original Length ◽  
Before And After ◽  
Cross Bridges

During vascular smooth muscle relaxation, myosin light-chain phosphorylation values decrease to resting values more rapidly than do stress values. Because phosphorylation is proportionally low, the latch-bridge hypothesis predicts that stress during relaxation should be predominantly carried by latch bridges. I evaluated the mechanical properties of latch bridges by changing tissue length and measuring myoplasmic Ca2+ concentration ([Ca2+]) with aequorin during relaxation of swine carotid medial tissues. Stress production was predicted with the latch-bridge model of Hai and Murphy, in which the measured aequorin [Ca2+] signal is the only determinant of stress. The aequorin-based latch-bridge model predicted relaxation induced by removal of the histamine stimulation. However, when tissues were relaxed by removal of extracellular Ca2+ or Ca(2+)-channel blockers in the continued presence of histamine, the aequorin-based model modestly underestimated the resulting relaxation. This underestimation was most likely caused by a small increase in the [Ca2+] sensitivity of phosphorylation since a model with an altered [Ca2+] sensitivity of phosphorylation more accurately predicted the resulting relaxation. The time course of relaxation in swine carotid artery was not substantially altered when the tissue was either briefly stretched or shortened and then returned to the original length. Because stretch should detach cross bridges, I modified the aequorin-based latch-bridge model to account for stretch-induced cross-bridge detachment. Because [Ca2+] values were slightly above resting values both before and after the stretch, the model predicted that phosphorylated cross bridges could reattach, be dephosphorylated, and form new latch bridges. The model predicted relaxation except during the first few seconds after stretch. These results suggest that latch-bridge reattachment is not necessary to explain the majority of the response to stretch during relaxation. The rate-limiting step for relaxation appears to be removal of [Ca2+] and not latch-bridge detachment.

Mechanical alterations in sensitized canine saphenous vein

1990 ◽  
Vol 69 (1) ◽  
pp. 171-178 ◽  
Author(s):  
Z. Wang ◽  
C. Y. Seow ◽  
W. Kepron ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Saphenous Vein ◽  
Specific Antigen ◽  
Isometric Tension ◽  
Antigen Challenge ◽  
Pollen Extract ◽  
Shortening Velocity ◽  
Tension Development ◽  
Cycling Rate ◽  
Cross Bridge

Because it is likely that antigen sensitization is not restricted to airway smooth muscle but probably involves all tissues in the animal, we decided to test the hypothesis that saphenous vein from pollen extract-sensitized dogs is sensitized and is, in addition, mechanically altered. To this end, we studied responses to specific antigen challenge and length-tension and force-velocity relationships in sensitized (SSV) and control saphenous veins (CSV). The antigen challenge revealed that the venous smooth muscle was strongly sensitized and developed a Schultz-Dale response, the two main mediators of which were histamine and norepinephrine. Length-tension relationship studies showed that whereas there is no difference in maximum isometric tension development between SSV and CSV [93.95 +/- 7.34 and 87.86 +/- 4.00 (SE) mN/mm2, respectively], SSV exhibited a significantly greater maximum isotonic shortening capacity of 0.613 +/- 0.009 optional length (lo) vs. 0.578 +/- 0.012 lo for CSV. Unloaded shortening velocity (Vo), which reflects the cross-bridge cycling rate, was determined at different times after the onset of electrical stimulation. Maximum Vo was attained early (5 s) in the contraction; a 15% decline in Vo was observed at the plateau of the contraction (15 s). At 5 s, Vo of SSV (0.316 +/- 0.019 lo/s) was significantly higher than that of CSV (0.269 +/- 0.018 lo/s), although Vos were same at 15 (0.249 +/- 0.021 lo/s for SSV and 0.237 +/- 0.019 lo/s for CSV). The increase in shortening likely results from th e increase in the early cross-bridge cycling rate because our studies show that the bulk of shortening occurs in the first 5 s.(ABSTRACT TRUNCATED AT 250 WORDS)

Time dependence of shortening velocity in tracheal smooth muscle

1986 ◽  
Vol 251 (3) ◽  
pp. C435-C442 ◽  
Author(s):  
N. L. Stephens ◽  
M. L. Kagan ◽  
C. S. Packer
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Shortening Velocity ◽  
Time Intervals ◽  
Activity Maximum ◽  
Cross Bridge ◽  
Cross Bridges ◽  
Latch State ◽  
Stimulation Of

It seems fairly well established that in the early phase of smooth muscle contraction cross bridges cycle at a relatively rapid rate. Later on these are replaced by very slowly cycling cross bridges or "latch bridges," operating with high economy. We describe a method to identify the time at which the transition occurs. By abruptly applying a light afterload at varying time intervals after stimulation of a canine tracheal smooth muscle, a point in time could be identified when cross-bridge cycling slowed. This was called the transition time. Because this transition was load dependent, the study was repeated with the preload abruptly reduced to zero. This permitted analysis of data in terms of cross-bridge activity. Maximum zero load velocity (Vo) of the contractile machinery was plotted against time and yielded a biphasic curve. The descending limb of the curve was fitted by a curve of the form Vo(t) = alpha e-K1t + beta e-K2t; K1 was almost three times greater than K2. We speculate that the faster rate constant represented activity of the early rapidly cycling cross bridges, and the slower constant reflected cycling rates in the latch state. These results are consistent with the latch bridge hypothesis put forward by Dillon et al. and enable us to provide a first approximation of the relative velocities of the two types of cross bridges.

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