Response of arterial smooth muscle to length perturbation

Seow, Chun Y.

doi:10.1152/jappl.2000.89.5.2065

Cited by 46 publications

(45 citation statements)

References 32 publications

(47 reference statements)

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“…Because muscle cell active tension is due to the transmission through cytoskeletal adhesion junctions of tension generated by actomyosin cross bridges, the proposed mechanisms for length adaptation of active tension include changes in actin and myosin polymerization leading to addition and subtraction of sarcomeres, and sarcomere and cytoskeletal adhesion junction reorganization (13,16,17,25). Although the most extensive work on length adaptation of active tension has been done on airway smooth muscle (12), there is also evidence of length adaptation of active tension in certain arteries (40,51), rabbit bladder (45), and cat ileum (3).…”

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confidence: 99%

Evidence that actomyosin cross bridges contribute to “passive” tension in detrusor smooth muscle

Ratz

Speich

2010

American Journal of Physiology-Renal Physiology

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Ratz PH, Speich JE. Evidence that actomyosin cross bridges contribute to "passive" tension in detrusor smooth muscle. Am J Physiol Renal Physiol 298: F1424 -F1435, 2010. First published April 7, 2010 doi:10.1152/ajprenal.00635.2009.-Contraction of detrusor smooth muscle (DSM) at short muscle lengths generates a stiffness component we termed adjustable passive stiffness (APS) that is retained in tissues incubated in a Ca 2ϩ -free solution, shifts the DSM length-passive tension curve up and to the left, and is softened by muscle strain and release (strain softened). In the present study, we tested the hypothesis that APS is due to slowly cycling actomyosin cross bridges. APS and active tension produced by the stimulus, KCl, displayed similar length dependencies with identical optimum length values. The myosin II inhibitor blebbistatin relaxed active tension maintained during a KCl-induced contraction and the passive tension maintained during stress-relaxation induced by muscle stretch in a Ca 2ϩ -free solution. Passive tension was attributed to tension maintaining rather than tension developing cross bridges because tension did not recover after a rapid 10% stretch and release as it did during a KCl-induced contraction. APS generated by a KCl-induced contraction in intact tissues was preserved in tissues permeabilized with Triton X-100. Blebbistatin and the actin polymerization inhibitor latrunculin-B reduced the degree of APS generated by a KCl-induced contraction. The degree of APS generated by KCl was inhibited to a greater degree than was the peak KCl-induced tension by rhoA kinase and cyclooxygenase inhibitors. These data support the hypothesis that APS is due to slowly cycling actomyosin cross bridges and suggest that cross bridges may play a novel role in DSM that uniquely serves to ensure proper contractile function over an extreme working length range. urinary bladder; muscle mechanics; Triton X-100 permeabilization; Rho-kinase

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confidence: 99%

Evidence that actomyosin cross bridges contribute to “passive” tension in detrusor smooth muscle

Ratz

Speich

2010

American Journal of Physiology-Renal Physiology

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“…For example, it is known that stretch could induce a contraction of smooth muscle referred to as myogenic response. The stretch-induced myogenic response is a recognized phenomenon in vascular smooth muscle (9,27). Induction of myogenic response has also been shown in guinea pig ASM, and this response could be abolished by inhibiting prostanoid release with indomethacin (11).…”

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confidence: 99%

Length oscillation induces force potentiation in infant guinea pig airway smooth muscle

Wang¹,

Chitano²,

Murphy³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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-Deep inspiration counteracts bronchospasm in normal subjects but triggers further bronchoconstriction in hyperresponsive airways. Although the exact mechanisms for this contrary response by normal and hyperresponsive airways are unclear, it has been suggested that the phenomenon is related to changes in force-generating ability of airway smooth muscle after mechanical oscillation. It is known that healthy immature airways of both humans and animals exhibit hyperresponsiveness. We hypothesize that the profile of active force generation after mechanical oscillation changes with maturation and that this change contributes to the expression of airway hyperresponsiveness in juveniles. We examined the effect of an acute sinusoidal length oscillation on the force-generating ability of tracheal smooth muscle from 1 wk, 3 wk, and 2-to 3-mo-old guinea pigs. We found that the length oscillation produced 15-20% initial reduction in active force equally in all age groups. This was followed by a force recovery profile that displayed striking maturation-specific features. Unique to tracheal strips from 1-wk-old animals, active force potentiated beyond the maximal force generated before oscillation. We also found that actin polymerization was required in force recovery and that prostanoids contributed to the maturation-specific force potentiation in immature airway smooth muscle. Our results suggest a potentiated mechanosensitive contractile property of hyperresponsive airway smooth muscle. This can account for further bronchoconstriction triggered by deep inspiration in hyperresponsive airways. actin polymerization; deep inspiration; hyperresponsive airways; ontogenesis; prostanoids AIRWAY HYPERRESPONSIVENESS is characterized by increased sensitivity of the tracheobronchial tree to contractile stimuli as well as an increased capacity for airway narrowing. Altered contractility of airway smooth muscle (ASM) is one of the mechanisms potentially responsible for increased airway sensitivity and maximal response. The involvement of ASM in the pathogenesis of airway hyperresponsiveness has long been controversial. However, both the capacity and velocity of shortening have been shown to be elevated in ASM from hyperresponsive airways (14,17). Increased ASM contractility shown in young animals suggests a central role for ASM also in juvenile airway hyperresponsiveness (8). It becomes, therefore, particularly important to study the mechanisms by which ASM function changes with maturation and whether this has a role in juvenile hyperresponsiveness and childhood asthma.An important feature of altered airway function in asthma is the inability of deep inspiration (DI) to improve airway function (37). DI could even induce bronchoconstriction in asthmatic subjects (2, 19). It has been convincingly shown that DI reverses bronchoconstriction in normal subjects by stretching contracted ASM (22). The protective effect of DI gained considerable research interest in recent years due to reports that showed a DI before the administration of a cont...

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“…The half-time for isometric stress recovery varies depending on the smooth muscle type used. Wang et al (2001) reported a half-time of 3-5 mins (depending on the length the specimen was adapted to) for rabbit airway smooth muscle while it was approximately 7 mins for rabbit carotid arteries, see Seow (2000). Comparing with Fig.…”

Section: Discussionmentioning

confidence: 87%

“…Finally, length adaptation operates on a time scale of minutes to hours (Pratusevich et al, 1995;Seow, 2000;Syyong et al, 2008) while maximum smooth muscle contraction can be achieved within seconds. This implies thatṅ ≈ 0 compared to the strain rate so thaṫ…”

Section: Kinematicsmentioning

confidence: 99%

Length adaptation of smooth muscle contractile filaments in response to sustained activation

Stålhand

Holzapfel

2016

Journal of Theoretical Biology

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Airway and bladder smooth muscles are known to undergo length adaptation under sustained contraction. This adaptation process entails a remodelling of the intracellular actin and myosin filaments which shifts the peak of the active force-length curve towards the current length. Smooth muscles are therefore able to generate the maximum force over a wide range of lengths. In contrast, length adaptation of vascular smooth muscle has attracted very little attention and only a handful of studies have been reported. Although their results are conflicting on the existence of a length adaptation process in vascular smooth muscle, it seems that, at least, peripheral arteries and arterioles undergo such adaptation. This is of interest since peripheral vessels are responsible for pressure regulation, and a length adaptation will affect the function of the cardiovascular system. It has, e.g., been suggested that the inward remodelling of resistance vessels associated with hypertension disorders may be related to smooth muscle adaptation. In this study we develop a continuum mechanical model for vascular smooth muscle length adaptation by assuming that the muscle cells remodel the actomyosin network such that the peak of the active stress-stretch curve is shifted towards the operating point. The model is specialised to hamster cheek pouch arterioles and the simulated response to stepwise length changes under contraction. The results show that the model is able to recover the salient features of length adaptation reported in the literature.

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Response of arterial smooth muscle to length perturbation

Cited by 46 publications

References 32 publications

Evidence that actomyosin cross bridges contribute to “passive” tension in detrusor smooth muscle

Evidence that actomyosin cross bridges contribute to “passive” tension in detrusor smooth muscle

Length oscillation induces force potentiation in infant guinea pig airway smooth muscle

Length adaptation of smooth muscle contractile filaments in response to sustained activation

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