Smooth muscle length-dependent PI(4,5)P2 synthesis and paxillin tyrosine phosphorylation

2001 ◽  
Vol 281 (1) ◽  
pp. C300-C310 ◽  
Author(s):  
Donggeun Sul ◽  
Carl B. Baron ◽  
Raymond Broome ◽  
Ronald F. Coburn
Keyword(s):  
Smooth Muscle ◽  
Phosphatidic Acid ◽  
Tyrosine Phosphorylation ◽  
Muscle Length ◽  
Time Dependent ◽  
Integrin Signaling ◽  
Optimal Length ◽  
Pi Turnover ◽  
Inositol Phospholipid ◽  
Trachealis Muscle

We studied effects of increasing the length of porcine trachealis muscle on 5.5 μM carbachol (CCh)-evoked phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] synthesis and other parameters of phosphatidylinositol (PI) turnover. PI(4,5)P2 resynthesis rates in muscle held at 1.0 optimal length ( L o), measured over the first 6 min of CCh stimulation, were 140 ± 12 and 227 ± 14% of values found in muscle held at 0.5 L o and in free-floating muscle, respectively. Time-dependent changes in cellular masses of PI(4,5)P2, PI, and phosphatidic acid, and PI resynthesis rates, were also altered by the muscle length at which contraction occurred. In free-floating muscle, CCh did not evoke increases in tyrosine-phosphorylated paxillin (PTyr-paxillin), an index of β1-integrin signaling; however, there were progressive increases in PTyr-paxillin in muscle held at 0.5 and 1.0 L o during contraction, which correlated with increases in PI(4,5)P2 synthesis rates. These data indicate that PI(4,5)P2 synthesis rates and other parameters of CCh-stimulated inositol phospholipid turnover are muscle length-dependent and provide evidence that supports the hypothesis that length-dependent β1-integrin signals may exert control on CCh-activated PI(4,5)P2synthesis.

Mechanical strain modulates maximal phosphatidylinositol turnover in airway smooth muscle

1999 ◽  
Vol 277 (5) ◽  
pp. L968-L974 ◽  
Author(s):  
Steven S. An ◽  
Chi-Ming Hai
Keyword(s):  
Smooth Muscle ◽  
G Proteins ◽  
Airway Smooth Muscle ◽  
Mechanical Strain ◽  
Muscle Length ◽  
Heterotrimeric G Proteins ◽  
Maximal Level ◽  
Optimal Length ◽  
Pi Turnover ◽  
Length Dependence

Mechanical strain regulates the maximal level of myosin light chain phosphorylation mediated by muscarinic activation in airway smooth muscle. Accordingly, we tested the hypothesis that mechanical strain regulates maximal phosphatidylinositol (PI) turnover ( V max) coupled to muscarinic receptors in bovine tracheal smooth muscle. We found that PI turnover was not significantly length dependent in unstimulated tissues. However, carbachol-induced PI turnover was linearly dependent on muscle length at both 1 and 100 μM. The observed linear length dependence of PI turnover at maximal carbachol concentration (100 μM) suggests that mechanical strain regulates V max. When carbachol concentration-PI turnover relationships were measured at optimal length and at 20% optimal length, the results could be explained by changes in V max alone. To determine whether the length-dependent step is upstream from heterotrimeric G proteins, we investigated the length dependence of fluoroaluminate-induced PI turnover. The results indicate that fluoroaluminate-induced PI turnover remained significantly length dependent at maximal concentration. These findings together suggest that regulating functional units of G proteins and/or phospholipase C enzymes may be the primary mechanism of mechanosensitive modulation in airway smooth muscle.

Selected Contribution: Effect of chronic passive length change on airway smooth muscle length-tension relationship

2001 ◽  
Vol 90 (2) ◽  
pp. 734-740 ◽  
Author(s):  
Lu Wang ◽  
Peter D. Paré ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Force Production ◽  
Muscle Length ◽  
Electrical Field Stimulation ◽  
Length Change ◽  
Electrical Field ◽  
Optimal Length ◽  
Active Length ◽  
Reference Length ◽  
Relationship Of

The ability of rabbit trachealis to undergo plastic adaptation to chronic shortening or lengthening was assessed by setting the muscle preparations at three lengths for 24 h in relaxed state: a reference length in which applied force was ∼1–2% of maximal active force (Po) and lengths considerably shorter and longer than the reference. Passive and active length-tension ( L-T) curves for the preparations were then obtained by electrical field stimulation at progressively increasing muscle length. Classically shaped L-T curves were obtained with a distinct optimal length ( L o) at which Podeveloped; however, both the active and passive L-T curves were shifted, whereas Po remained unchanged. L o was 72% and 148% that of the reference preparations for the passively shortened and lengthened muscles, respectively. The results suggest that chronic narrowing of the airways could induce a shift in the L-T relationship of smooth muscle, resulting in a maintained potential for maximal force production.

Tracheal smooth muscle mechanics in vivo

1990 ◽  
Vol 68 (1) ◽  
pp. 209-219 ◽  
Author(s):  
M. Okazawa ◽  
P. Pare ◽  
J. Road
Keyword(s):  
Smooth Muscle ◽  
Muscle Mechanics ◽  
Muscle Length ◽  
Base Line ◽  
Maximal Velocity ◽  
Velocity Of Shortening ◽  
Length Changes ◽  
Trachealis Muscle

We applied the technique of sonomicrometry to directly measure length changes of the trachealis muscle in vivo. Pairs of small 1-mm piezoelectric transducers were placed in parallel with the muscle fibers in the posterior tracheal wall in seven anesthetized dogs. Length changes were recorded during mechanical ventilation and during complete pressure-volume curves of the lung. The trachealis muscle showed spontaneous fluctuations in base-line length that disappeared after vagotomy. Before vagotomy passive pressure-length curves showed marked hysteresis and length changed by 18.5 +/- 13.2% (SD) resting length at functional residual capacity (LFRC) from FRC to total lung capacity (TLC) and by 28.2 +/- 16.2% LFRC from FRC to residual volume (RV). After vagotomy hysteresis decreased considerably and length now changed by 10.4 +/- 3.7% LFRC from FRC to TLC and by 32.5 +/- 14.6% LFRC from FRC to RV. Bilateral supramaximal vagal stimulation produced a mean maximal active shortening of 28.8 +/- 14.2% resting length at any lung volume (LR) and shortening decreased at lengths above FRC. The mean maximal velocity of shortening was 4.2 +/- 3.9% LR.S-1. We conclude that sonomicrometry may be used to record smooth muscle length in vivo. Vagal tone strongly influences passive length change. In vivo active shortening and velocity of shortening are less than in vitro, implying that there are significant loads impeding shortening in vivo.

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.

In vivo loads on airway smooth muscle: the role of noncontractile airway structures

1992 ◽  
Vol 70 (4) ◽  
pp. 602-606 ◽  
Author(s):  
Philip Robinson ◽  
Mitsushi Okazawa ◽  
Tony Bai ◽  
Peter Paré
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Activation ◽  
Muscle Length ◽  
Tracheal Cartilage ◽  
Elastic Load ◽  
Muscle Shortening ◽  
Trachealis Muscle

The degree of airway smooth muscle contraction and shortening that occurs in vivo is modified by many factors, including those that influence the degree of muscle activation, the resting muscle length, and the loads against which the muscle contracts. Canine trachealis muscle will shorten up to 70% of starting length from optimal length in vitro but will only shorten by around 30% in vivo. This limitation of shortening may be a result of the muscle shortening against an elastic load such as could be applied by tracheal cartilage. Limitation of airway smooth muscle shortening in smaller airways may be the result of contraction against an elastic load, such as could be applied by lung parenchymal recoil. Measurement of the elastic loads applied by the tracheal cartilage to the trachealis muscle and by lung parenchymal recoil to smooth muscle of smaller airways were performed in canine preparations. In both experiments the calculated elastic loads applied by the cartilage and the parenchymal recoil explained in part the limitation of maximal active shortening and airway narrowing observed. We conclude that the elastic loads provided by surrounding structures are important in determining the degree of airway smooth muscle shortening and the resultant airway narrowing.Key words: elastic loads, tracheal cartilage, airway smooth muscle shortening.

scholarly journals Relationship between stimulated phosphatidic acid production and inositol lipid hydrolysis in intestinal longitudinal smooth muscle from guinea pig

1987 ◽  
Vol 244 (3) ◽  
pp. 763-768 ◽  
Author(s):  
R S E Mallows ◽  
T B Bolton
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Phosphatidic Acid ◽  
Inositol Phosphates ◽  
Muscle Layer ◽  
Phospholipid Hydrolysis ◽  
Longitudinal Smooth Muscle ◽  
Inositol Phospholipid

Accumulation of [32P]phosphatidic acid (PA) and total [3H]inositol phosphates (IPs) was measured in the longitudinal smooth-muscle layer from guinea-pig small intestine. Stimulation with carbachol, histamine and substance P produced increases in accumulation of both [3H]IPs and [32P]PA over the same concentration range. The increase in [32P]PA accumulation in response to carbachol (1 microM-0.1 mM) was inhibited in the presence of atropine (0.5 microM). Buffering the external free [Ca2+] to 10 nM did not prevent the carbachol-stimulated increase in [32P]PA accumulation. Carbachol and Ca2+ appear to act synergistically to increase accumulation of [32P]PA. In contrast, although incubation with noradrenaline also increased accumulation of [3H]IPs, no increase in accumulation of [32P]PA could be detected. These results suggest that an increase in formation of IPs is not necessarily accompanied by an increase in PA formation, and imply the existence of receptor-modulated pathways regulating PA concentrations other than by phospholipase-C-catalysed inositol phospholipid hydrolysis.

Stretch-induced membrane depolarization in ferret trachealis smooth muscle cells

1987 ◽  
Vol 62 (6) ◽  
pp. 2320-2325 ◽  
Author(s):  
R. F. Coburn
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Length ◽  
Membrane Depolarization ◽  
Muscle Membrane ◽  
Induced Membrane ◽  
Length Increase ◽  
Smooth Muscle Membrane ◽  
Per Se ◽  
Trachealis Muscle

We determined the effects of increasing the length of the ferret trachealis muscle on smooth muscle membrane potentials recorded on successive impalements by microelectrodes. The preparation included the paratracheal ganglion nerve plexus as well as trachealis muscle. With sustained increases in muscle length over the range 0.5–0.8 to 1.2 maximal length (Lmax), depolarization occurred, which was related to the amplitude of the length increase. Membrane depolarizations were also evoked after stretching to lengths approximately 1.1 Lmax and returning to the control length. Stretch-induced membrane depolarizations developed after the stretch maneuver was complete; were slowly reversible; were not influenced by tetrodotoxin or atropine; were related to stretch rather than to maintained increase in muscle length; were not transmitted to adjacent nonstretched segments of the trachea; and were often associated with slow waves which appear to be secondary to membrane depolarization rather than stretch per se.

Quantitative measurement of smooth muscle shortening in isolated pig trachea

1987 ◽  
Vol 63 (4) ◽  
pp. 1360-1365 ◽  
Author(s):  
A. L. James ◽  
P. D. Pare ◽  
R. H. Moreno ◽  
J. C. Hogg
Keyword(s):  
Smooth Muscle ◽  
Quantitative Measurement ◽  
Muscle Length ◽  
Tracheal Ring ◽  
Wall Area ◽  
Intact Cartilage ◽  
Muscle Shortening ◽  
Inner Surface ◽  
Outer Border ◽  
Trachealis Muscle

Matched porcine tracheal rings were exposed to theophylline and increasing doses of carbachol in Krebs solution. Histological sections of each ring were traced and each of the following dimensions measured: the external perimeter (Pe) and external area (Ae) defined by the outer border of smooth muscle and inner surface of cartilage, and the internal perimeter (Pi) and internal area (Ai) defined by the luminal surface of the epithelium and the muscle length (L) along its outer border. Absolute wall area (WA = Ae - Ai) and relative wall area (PW = WA/Ae) were calculated. Carbachol-treated tracheal ring dimensions were compared with those of their matched theophylline-treated rings. In tracheal rings with intact cartilage, maximal smooth muscle shortening of 44% was achieved with 10(-2) M carbachol. In tracheal rings in which anterior and posterior segments of cartilage were excised, the trachealis muscle passively shortened by 20% and maximal shortening (10(-3) M carbachol) was 57%. Although Ai decreased with maximal smooth muscle shortening, there were no changes in the length of Pi or in WA. These data show that the cartilage in the porcine trachea exerts both a preload that passively stretches the trachealis muscle and an afterload that limits maximal smooth muscle shortening.

Length-dependent regulation of basal myosin phosphorylation and force in detrusor smooth muscle

2003 ◽  
Vol 284 (4) ◽  
pp. R1063-R1070 ◽  
Author(s):  
Paul H. Ratz ◽  
Amy S. Miner
Keyword(s):  
Smooth Muscle ◽  
Myosin Light Chain ◽  
Muscle Length ◽  
Detrusor Smooth Muscle ◽  
Optimal Length ◽  
Kinase C ◽  
Rhoa Kinase ◽  
Filling Phase ◽  
Bladder Detrusor

Urinary bladder (detrusor) smooth muscle is active in the absence of an external stimulus. Tone occurs even “at rest” during the filling phase, and it is elevated in patients with overactive bladder. This study examined the role of muscle length on tone and the level of basal myosin light chain phosphorylation (MLC20P). MLC20P was 23.9 ± 1% ( n = 58) at short lengths (zero preload; L z). An increase in length from L z to the optimal length for contraction ( L o) caused a reduction in MLC20P to 15.8 ± 1% ( n = 49). Whereas 10 μM staurosporine reduced MLC20P at L z, 1 μM staurosporine, a Ca2+-free solution, and inhibitors of MLC kinase, protein kinase C (PKC) and RhoA kinase (ROK) did not. However, 1 μM staurosporine and inhibitors of ROK inhibited MLC20P and tone at L o. These data support the hypothesis that a Ca2+-independent kinase, possibly ZIP-like kinase, regulates MLC20P at L z, whereas in detrusor stretched to L o, additional kinases, such as ROK, participate.

scholarly journals Mechanical signals and mechanosensitive modulation of intracellular [Ca2+] in smooth muscle

2000 ◽  
Vol 279 (5) ◽  
pp. C1375-C1384 ◽  
Author(s):  
Steven S. An ◽  
Chi-Ming Hai
Keyword(s):  
Smooth Muscle ◽  
Isometric Force ◽  
Muscle Length ◽  
Cyclopiazonic Acid ◽  
Underlying Mechanism ◽  
Optimal Length ◽  
Mechanical Signal ◽  
Intracellular Ca ◽  
Data Points ◽  
Isotonic Shortening

We tested the hypothesis that strain is the primary mechanical signal in the mechanosensitive modulation of intracellular Ca2+concentration ([Ca2+]i) in airway smooth muscle. We found that [Ca2+]i was significantly correlated with muscle length during isotonic shortening against 20% isometric force (Fiso). When the isotonic load was changed to 50% Fiso, data points from the 20 and 50% Fiso experiments overlapped in the length-[Ca2+]i relationship. Similarly, data points from the 80% Fiso experiments clustered near those from the 50% Fiso experiments. Therefore, despite 2.5- and 4-fold differences in external load, [Ca2+]idid not deviate much from the length-[Ca2+]irelation that fitted the 20% Fiso data. Maximal inhibition of sarcoplasmic reticular (SR) Ca2+ uptake by 10 μM cyclopiazonic acid (CPA) did not significantly change [Ca2+]i in carbachol-induced isometric contractions and isotonic shortening. CPA also did not significantly change myosin light-chain phosphorylation or force redevelopment when carbachol-activated muscle strips were quickly released from optimal length ( L o) to 0.5 L o. These results are consistent with the hypothesis and suggest that SR Ca2+ uptake is not the underlying mechanism.

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