Tension Development (tension + development)

Distribution by Scientific Domains

Selected Abstracts

Caffeine administration results in greater tension development in previously fatigued canine muscle in situ

Richard A. Howlett
In isolated single skeletal myocytes undergoing long-term fatiguing contractions, caffeine (CAF) can result in nearly immediate restoration of generated tension to near-prefatigue levels by increasing Ca2+ release via activation of sarcoplasmic reticulum release channels. This study tested whether arterial CAF infusion (>5 mm) would cause a similar rapid restoration of tetanic isometric tension during contractions to fatigue in perfused canine hindlimb muscle in situ. Tetanic contractions were elicited by electrical stimulation (200 ms trains, 50 Hz, 1 contraction s,1), and biopsies were taken from the muscle at rest and during contractions: (1) following the onset of fatigue (tension ,60% of initial value); and (2) following CAF administration. Resting muscle ATP, PCr and lactate contents were 25.2 ± 0.4, 76.9 ± 3.3 and 14.4 ± 3.3 mmol (kg dry weight),1, respectively. At fatigue, generated tetanic tension was 61.1 ± 6.9% of initial contractions. There was a small but statistically significant recovery of tetanic tension (64.9 ± 6.6% of initial value) with CAF infusion, after which the muscle showed incomplete relaxation. At fatigue, muscle ATP and PCr contents had fallen significantly (P < 0.05) to 18.1 ± 1.1 and 18.9 ± 2.1 mmol (kg dry weight),1, respectively, and lactate content had increased significantly to 27.7 ± 5.4 mmol (kg dry weight),1. Following CAF, skeletal muscle ATP and PCr contents were significantly lower than corresponding fatigue values (15.0 ± 1.3 and 10.9 ± 2.2 mmol (kg dry weight),1, respectively), while lactate was unchanged (22.2 ± 3.9 mmol (kg dry weight),1). These results demonstrate that caffeine can result in a small, but statistically significant, recovery of isometric tension in fatigued canine hindlimb muscle in situ, although not nearly to the same degree as seen in isolated single muscle fibres. This suggests that, in this in situ isolated whole muscle model, alteration of Ca2+ metabolism is probably only one cause of fatigue. [source]

Surface Action Potential and Contractile Properties of the Human Triceps Surae Muscle: Effect of ,Dry' Water Immersion

Yuri A. Koryak
The effects of 7 days of ,dry' water immersion were investigated in six subjects. Changes in the contraction properties were studied in the triceps surae muscle. After immersion, the maximal voluntary contraction (MVC) was reduced by 18.9% (P < 0.01), and the electrically evoked (150 impulses s,1) maximal tension during tetanic contraction (Po) was reduced by 8.2% (P > 0.05). The difference between Po and MVC expressed as a percentage of Po and referred to as force deficiency was also calculated. The force deficiency increased by 44.1% (P < 0.001) after immersion. The decrease in Po was associated with increased maximal rates of tension development (7.2%) and relaxation. The twitch time-to-peak was not significantly changed, and half-relaxation and total contraction time were decreased by 5.3% and 2.8%, respectively, but the twitch tension (Pt) was not significantly changed and the Pt/Po ratio was decreased by 8.7%. The 60 s intermittent contractions (50 impulses s,1) decreased tetanic force to 57% (P < 0.05) of initial values, but force reduction was not significantly different in the two fatigue-inducing tests: fatigue index (the mean loss of force of the last five contractions, expressed as a percentage of the mean value of the first five contractions) was 36.2 ± 5.4% vs. 38.6 ± 2.8%, respectively (P > 0.05). While identical force reduction was present in the two fatigue-inducing tests, it would appear that concomitant electrical failure was considerably different. Comparison of the electrical and mechanical alterations recorded during voluntary contractions, and in contractions evoked by electrical stimulation of the motor nerve, suggests that immersion not only modifies the peripheral processes associated with contraction, but also changes central and/or neural command of the contraction. At peripheral sites, it is proposed that the intracellular processes of contraction play a role in the contractile impairment recorded during immersion. [source]

Effects of ouabain on contractions induced by manganese ions in Ca2+ -free, isotonic solutions with varying concentrations of K+ in guinea-pig taenia coli

Tetsuyuki Nasu
Abstract The action of ouabain, a cell membrane Na+, K+ -ATPase blocker, on contractions induced by manganese ions (Mn2+) in Ca2+ -free, isotonic solutions with varying concentrations of K+ in the external medium were investigated in order to evaluate the underlying role of external Na+ in Mn2+ -induced contractions in isolated taenia coli of the guinea-pig. Mn2+ at 5 mm induced greater contractions as external isotonic K+ concentrations progressively increased from 10 to 100 mm. Ouabain (2 × 10,4 m) completely inhibited tension development stimulated by 5 mm Mn2+ in isotonic, 30 mm K+ (96 mm Na+) medium. Whereas, the tension inhibitory effects of ouabain became progressively weaker as isotonic, external K+ concentrations increased to 60 mm, which successively decreased external Na+ concentrations. Eventually, ouabain failed to affect contractions stimulated by Mn2+ in isotonic, 126 mm K+, Na+ -deficient medium. Ouabain caused progressively greater increase in cellular Na+ concentrations as the Na+ concentrations increased in the isotonic, K+ medium. While, pyruvate, which penetrates cell independently of external Na+, reversed the inhibition of tension by ouabain in isotonic, 30 mm K+, Na+ -sufficient (96 mm) medium containing 5 mm Mn2+. These results suggested that Mn2+ induced the contraction, which was maintained by glucose transport depending on external Na+, in the case of Na+ -sufficient medium in K+ -depolarized taenia coli. However, it induced the contraction independent of external Na+, in the case of Na+ -deficient, K+ medium. Ouabain might exhibit greater inhibition of the contraction induced by Mn2+ as the decrease in the Na+ gradient across the cell membranes continues. [source]

Role of Repolarization Restitution in the Development of Coarse and Fine Atrial Fibrillation in the Isolated Canine Right Atria

Introduction: Although the role of action potential duration restitution (APD-R) in the initiation and maintenance of ventricular fibrillation (VF) has been the subject of numerous investigations, its role in the generation of atrial fibrillation (AF) is less well studied. The cellular and ionic basis for coarse versus fine AF is not well delineated. Methods and Results: We measured APD-R during acetylcholine-mediated AF as well as during pacing (standard and dynamic protocols) in crista teriminalis, pectinate muscle, superior vena cava, and appendage of isolated canine arterially perfused right atria (n = 15). Transmembrane action potential (TAP), pseudo-ECG, and isometric tension development were simultaneously recorded. Acetylcholine flattened APD-R measured by both standard and dynamic protocols, but promoted induction of AF. AF was initially coarse, converting to fine within 3,15 minutes of AF. Coarse, but not fine AF was associated with dramatic fluctuations in tension development, reflecting wide variations in intracellular calcium activity ([Ca2+]i). During coarse AF, APD-R data displayed a cloud-like distribution pattern, with a wide range of maximum APD-R slope (from 1.21 to 0.35). A maximum APD-R slope >1 was observed only in crista terminalis (3/10). The APD-R relationship was relatively linear and flat during fine AF. Reduction of [Ca2+]i was associated with fine AF whereas augmentation of [Ca2+]i with coarse AF. Conclusions: Our data indicate that while APD-R may have a limited role in the maintenance of coarse AF, it is unlikely to contribute to the maintenance of fine AF and that [Ca2+]i dynamics determine the degree to which AF is coarse or fine. [source]

Relationship Between Regional Shortening and Asynchronous Electrical Activation in a Three-Dimensional Model of Ventricular Electromechanics

Introduction: Asynchronous electrical activation can cause abnormalities in perfusion and pump function. An electromechanical model was used to investigate the mechanical effects of altered cardiac activation sequence. Methods and Results: We used an anatomically detailed three-dimensional computational model of the canine ventricular walls to investigate the relationship between regional electrical activation and the timing of fiber shortening during normal and ventricular paced beats. By including a simplified Purkinje fiber network and anisotropic impulse conduction in the model, computed electrical activation sequences were consistent with experimentally observed patterns. Asynchronous time courses of regional strains during beats stimulated from the left or right ventricular epicardium showed good agreement with published experimental measurements in dogs using magnetic resonance imaging tagging methods. When electrical depolarization in the model was coupled to the onset of local contractile tension development by a constant time delay of 8 msec, the mean delay from depolarization to the onset of systolic fiber shortening was 14 msec. However, the delay between the onset of fiber tension and initial shortening varied significantly; it was as late as 60 msec in some regions but was also as early as ,50 msec (i.e., 42 msec before depolarization) in other regions, particularly the interventricular septum during free-wall pacing. Conclusion: The large variation in delay times was attributable to several factors including local anatomic variations, the location of the site relative to the activation wavefront, and regional end-diastolic strain. Therefore, we conclude that these factors, which are intrinsic to three-dimensional ventricular function, make the regional sequence of fiber shortening an unreliable surrogate for regional depolarization or electromechanical activation in the intact ventricles. (J Cardiovasc Electrophysiol, Vol. 14, pp. S196-S202, October 2003, Suppl.) [source]

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

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]

The effect of streptozotocin-induced diabetes on cardiac ,-adrenoceptor subtypes in the rat

D. J. Sellers
1,The present study investigates the effect of short-term experimental diabetes of 14-days duration on the ,-adrenoceptor subtypes of the rat heart. 2,,-adrenoceptor-mediated functional responses to submaximal doses of isoprenaline were enhanced in Langendorff-perfused hearts from diabetic rats, manifested as greater changes in tension, heart rate and rates of tension development (+dT/dt) and decline (,dT/dt). 3,Radioligand binding data demonstrated that total cardiac ,-adrenoceptor density and affinity for [3H]-dihydroalprenolol was unchanged by diabetes, although a decrease in ,1 -adrenoceptor density and increase in ,2 -adrenoceptor density was observed. 4,In conclusion, hearts from 14-day streptozotocin-induced diabetic rats demonstrate a number of alterations within the ,-adrenoceptor system. However, the enhanced ,-adrenoceptor-mediated responses to isoprenaline were not caused by an overall increase in density of ,-adrenoceptors, but were accompanied by changes in the ratio of the ,-adrenoceptor subtypes. [source]

Thrombin activation of proteinase-activated receptor 1 potentiates the myofilament Ca2+ sensitivity and induces vasoconstriction in porcine pulmonary arteries

Jun Maki
Background and purpose:, Thrombus formation is commonly associated with pulmonary arterial hypertension (PAH). Thrombin may thus play an important role in the pathogenesis and pathophysiology of PAH. Hence, we investigated the contractile effects of thrombin and its mechanism in pulmonary artery. Experimental approach:, The cytosolic Ca2+ concentrations ([Ca2+]i), 20 kDa myosin light chain (MLC20) phosphorylation and tension development were evaluated using the isolated porcine pulmonary artery. Key results:, Thrombin induced a sustained contraction in endothelium-denuded strips obtained from different sites of a pulmonary artery, ranging from the main pulmonary artery to the intrapulmonary artery. In the presence of endothelium, thrombin induced a transient relaxation. The contractile effect of thrombin was abolished by either a protease inhibitor or a proteinase-activated receptor 1 (PAR1) antagonist, while it was mimicked by PAR1 -activating peptide (PAR1AP), but not PAR4AP. The thrombin-induced contraction was associated with a small elevation of [Ca2+]i and an increase in MLC20 phosphorylation. Thrombin and PAR1AP induced a greater increase in tension for a given [Ca2+]i elevation than that obtained with high K+ -depolarization. They also induced a contraction at a fixed Ca2+ concentration in ,-toxin-permeabilized preparations. Conclusions and implications:, The present study revealed a unique property of the pulmonary artery. In contrast to normal arteries of the systemic circulation, thrombin induces a sustained contraction in the normal pulmonary artery, by activating PAR1 and thereby increasing the sensitivity of the myofilament to Ca2+. This responsiveness of the pulmonary artery to thrombin may therefore contribute to the pathogenesis and pathophysiology of PAH. [source]

Theophylline attenuates Ca2+ sensitivity and modulates BK channels in porcine tracheal smooth muscle

Shinji Ise
Theophylline, a nonselective phosphodiesterase inhibitor, has long been regarded as a major bronchodilator in the treatment of human asthma. Using front-surface fluorometry with fura-2 and , -toxin permeabilization, the effects of theophylline on intracellular Ca2+ concentration ([Ca2+]i), tension development and Ca2+ sensitivity of the contractile apparatus were investigated in porcine tracheal smooth muscle strips. Application of theophylline induced a relaxation without a significant decrease in [Ca2+]i when strips were precontracted by 40 mM K+ depolarization, while theophylline significantly decreased both [Ca2+]i and tension induced by carbachol. The effects of theophylline on the increases in [Ca2+]i and tension induced by carbachol were significantly inhibited by iberiotoxin, an inhibitor of large-conductance Ca2+ -activated K+ channels. In the absence of extracellular Ca2+, theophylline significantly attenuated carbachol-induced transient increases in tension development, while it did not affect carbachol-induced transient increase in [Ca2+]i. The [Ca2+]i,force relationship, which was determined by cumulative applications of extracellular Ca2+ (0,5 mM) during 40 mM K+ depolarization, was significantly shifted to the right by theophylline. In , -toxin permeabilized strips, theophylline significantly increased the EC50 value of [Ca2+]i for contraction and enhanced the effect of cAMP, but not of cGMP. These results indicate that theophylline induces relaxation of the porcine tracheal smooth muscle through an activation of BK channels, and a resultant decrease in [Ca2+]i and an attenuation of Ca2+ sensitivity, presumably through the action of cAMP. British Journal of Pharmacology (2003) 140, 939,947. doi:10.1038/sj.bjp.0705508 [source]

Effect of caffeine on response of rabbit isolated corpus cavernosum to high K+ solution, noradrenaline and transmural electrical stimulation

Adebowale Adebiyi
Summary 1.,Caffeine has wide-ranging activities on smooth muscles, including contractile and relaxant effects. The aim of the present study was to examine the activity of caffeine on rabbit corpus cavernosum (RCC). 2.,The effects of caffeine (0.5,4.0 mmol/L) on the response of RCC to high K+ solution, noradrenaline (NA) and transmural electrical stimulation (EFS) were studied in a tissue bath system. 3.,Caffeine did not contract the RCC. However, 0.5,4.0 mmol/L caffeine caused concentration-dependent relaxation of tension development in high-K+ (120 mmol/L) solution in contrast with the solvent control. At 4.0 mmol/L caffeine, high-K+ solution-induced tone of the RCC was reduced by 73.4 ± 7.3%. Caffeine (0.5,4.0 mmol/L) also concentration-dependently relaxed NA (12.5 µmol/L)-induced tonic contraction of the RCC. At 4.0 mmol/L caffeine, NA-induced tone of the RCC was reduced by 41.1 ± 7.0%. Incubation of RCC in 2.0 mmol/L caffeine for 30 min prior to EFS (1,40 Hz) caused a marked rightward shift in the frequency,response curve. 4.,The results of the present study suggest that caffeine exhibits relaxant activity on rabbit cavernosal smooth muscle and the mechanism of this activity possibly involves inhibition of Ca2+ signalling. [source]