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Active Tension (active + tension)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

Myometrial mechanoadaptation during pregnancy: implications for smooth muscle plasticity and remodelling

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2008
X. Wu
Abstract The smooth muscle of the uterus during pregnancy presents a unique circumstance of physiological mechanotransduction as the tissue remodels in response to stretches imposed by the growing foetus(es), yet the nature of the molecular and functional adaptations remain unresolved. We studied, in myometrium isolated from non-pregnant (NP) and pregnant mice, the active and passive length,tension curves by myography and the expression and activation by immunoblotting of focal adhesion-related proteins known in other systems to participate in mechanosensing and mechanotransduction. In situ uterine mass correlated with pup number and weight throughout pregnancy. In vitro myometrial active, and passive, length-tension curves shifted significantly to the right during pregnancy indicative of altered mechanosensitivity; at term, maximum active tension was generated following 3.94 ± 0.33-fold stretch beyond slack length compared to 1.91 ± 0.12-fold for NP mice. Moreover, mechanotransduction was altered during pregnancy as evidenced by the progressive increase in absolute force production at each optimal stretch. Pregnancy was concomitantly associated with an increased expression of the dense plaque-associated proteins FAK and paxillin, and elevated activation of FAK, paxillin, c-Src and extracellular signal-regulated kinase (ERK1/2) which reversed 1 day post-partum. Electron microscopy revealed close appositioning of neighbouring myometrial cells across a narrow extracellular cleft adjoining plasmalemmal dense plaques. Collectively, these results suggest a physiological basis of myometrial length adaptation, long known to be a property of many smooth muscles, whereupon plasmalemmal dense plaque proteins serve as molecular signalling and structural platforms contributing to functional (contractile) remodelling in response to chronic stretch. [source]

Ischemia,Reperfusion Impairs Ascending Vasodilation in Feed Arteries of Hamster Skeletal Muscle

MICROCIRCULATION, Issue 7 2005
MIRIAM C. J. DE WITH
ABSTRACT Objective: Vasodilation originating within the microcirculation ascends into proximal feed arteries during muscle contraction to attain peak levels of muscle blood flow. Ascending vasodilation (AVD) requires an intact endothelium, as does conducted vasodilation in response to acetylcholine (ACh). Whereas ischemia,reperfusion (I-R) can affect endothelial cell function, the effect of I-R on AVD is unknown. The authors tested the hypothesis that I-R (1h,1h) would impair AVD. Methods: Using the retractor muscle of anesthetized hamsters, contractions were evoked using field stimulation (200 ms at 40 Hz every 2 s for 1 min) and ACh was delivered using microiontophoresis (1 ,m tip, 500,4000 ms pulse at 800 nA). Feed artery responses were monitored 500,1500 ,m upstream. Results: Neither resting (51 ± 4 ,m) nor maximal diameter (81 ± 5 ,m; 10 ,m sodium nitroprusside) following I-R (n = 8) were different from time-matched controls (n = 10). With peak active tension of 23 ± 4 mN · mm,2, control AVD was 26 ± 2 ,m. Following I-R, active tension fell by 48% (p < .05) and AVD by 57% (p < .05). Stimulation at 70 Hz restored active tension but AVD remained depressed by nearly half (p < .05), as did local and conducted responses to ACh. Nevertheless, control responses to 500 ms ACh were restored by increasing stimulus duration to 4000 ms. Conclusions: Ischemia,reperfusion impairs the initiation of feed artery dilation with muscle contraction and with ACh while conduction along the vessel wall is preserved. Respective components of endothelial cell signaling events may differ in their susceptibility to I-R. [source]

Dynamic association between ,-actinin and ,-integrin regulates contraction of canine tracheal smooth muscle

THE JOURNAL OF PHYSIOLOGY, Issue 3 2006
Wenwu Zhang
The adhesion junctions of smooth muscle cells may be dynamically regulated during smooth muscle contraction, and this dynamic regulation may be important for the development of active tension. In the present study, the role of ,-actinin during smooth muscle contraction was evaluated in tracheal smooth muscle tissues and freshly dissociated cells. Stimulation with acetylcholine (ACh) increased the localization of ,-actinin at the membrane of freshly dissociated smooth muscle cells, and increased the amount of ,1 integrin that coprecipitated with ,-actinin from muscle tissue homogenates. GFP-,-actinin fusion proteins were expressed in muscle tissues and visualized in live freshly dissociated cells. GFP-,-actinin translocated to the membrane within seconds of stimulation of the cells with ACh. Expression of the integrin-binding rod domain of ,-actinin in smooth muscle tissues depressed active contraction in response to ACh. Expression of the ,-actinin rod domain also inhibited the translocation of endogenous ,-actinin to the membrane, and inhibited the association of endogenous ,-actinin with ,1 -integrin in ,-actinin immunoprecipitates from tissue extracts. However, the expression of ,-actinin rod domain peptides did not inhibit increases in myosin light chain phosphorylation or actin polymerization in response to stimulation with ACh. Results suggest that contractile stimulation of smooth muscle causes the rapid recruitment of ,-actinin to ,-integrin complexes at the membrane, and that the recruitment of ,-actinin to integrin complexes is necessary for active tension development in smooth muscle. [source]

Arteriolar network architecture and vasomotor function with ageing in mouse gluteus maximus muscle

THE JOURNAL OF PHYSIOLOGY, Issue 2 2004
Shawn E. Bearden
Physical diminishes with ageing, but little is known of how the microvascular supply to skeletal muscle fibres is affected. To test the hypothesis that ageing alters blood flow control, we investigated network architecture and vasomotor responses of arterioles in the gluteus maximus muscle of young (2,3 months), adult (12,14 months) and old (18,20 months) C57BL6 male mice (n= 83) (Young, Adult and Old, respectively). Microvascular casts revealed that the total number, length and surface area of arteriolar segments (diameter, 10,50 ,m) were not significantly different across age-groups. However, for arterioles with diameter of 30 ,m, tortuosity and branch angles increased with age (P < 0.05). In anaesthetized mice, second-order (2A) distributing arterioles had similar resting (17 ± 1 ,m) and maximal (37 ± 1 ,m) diameters and similar responsiveness to cumulative (10,10,10,4m) superfusion of acetylcholine or phenylephrine. With superfusate oxygen level raised from 0 to 21%, 2A arteriolar constriction in Young (11 ± 1 ,m) was greater (P < 0.05) than Adult and Old (5 ± 1 ,m). Observed 1 mm upstream from microiontophoresis of ACh (1 ,A, 1 s), conducted vasodilatation was 10 ± 1 ,m in Young, 17 ± 1 ,m in Adult and 6 ± 1 ,m in Old (P < 0.05). With muscle contractions (2, 4 and 8 Hz; 30 s) arteriolar diameter increased similarly across age-groups (6 ± 1, 11 ± 1 and 18 ± 1 ,m, respectively). Muscle mass and active tension were similar across age-groups yet postcontraction vasodilatation recovered more rapidly in Old versus Adult and Young (P < 0.05). With arteriolar network architecture maintained during ageing, the impairment in conducted vasodilatation and attenuation of postcontraction vasodilatation may compromise exercise tolerance. [source]