PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Muscle Contraction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources
PubMed1981

Effect of histamine on smooth-muscle contractions induced by noradrenaline and acetylcholine.

The effects of different histamine concentrations (1 X 10(-6) to 1 X 10(-4)M) on the contractile effects of noradrenaline and acetylcholine are studied on isolated smooth-muscle preparations from rats. Histamine, applied in concentrations of 1 X 10(-5)M and 1 X 10(-4)M, markedly potentiates the contractile effects of the lower concentrations of acetylcholine on the anococcygeal muscle, without essentially changing the maximum contractions induced by it. Histamine reduces 6.5-31.6 times the acetylcholine concentrations causing 50 per cent of the maximal contractions of this smooth-muscle preparation. Application of histamine on anococcygeal muscle decreases contractile responses to noradrenaline. A dependence is found between the histamine concentration used and the shift to the right of the curve "log concentration-effect" for noradrenaline. Histamine increases 2.6 to 16.2 times the noradrenaline concentrations needed for inducing 50 per cent of the maximum contractile response of the anococcygeal muscle. The interaction between noradrenaline and histamine on this smooth-muscle preparation is not competitive. Histamine in the concentrations applied does not influence the contractile effects of noradrenaline on vas deferens and of acetylcholine on tracheal smooth-muscle preparation. In rat anococcygeal muscle histamine most probably influences the contractile effects of noradrenaline and acetylcholine through allosteric interaction with their receptors.

Acetylcholine↗
PubMed2002

Effects of interleukin-18 on diaphragm muscle contraction on rats.

To evaluate the role of interleukin (IL)-18 in endotoxin-induced diaphragm muscle deterioration, we studied three treatment groups, namely, a saline+endotoxin group, an IL-18+endotoxin group and an IL-18 only group using Wistar rats. Five minutes after saline or IL-18 (0.25 microg) injection, E. coli endotoxin (30 mg/kg) was injected intraperitoneally. In the saline+endotoxin group, the force-frequency curves by ANOVA (p < 0.01), twitch tension (TT) and slope during contraction time (TT/CT) were significantly lower at 4 hours than those at 0 hours due to endotoxin (p < 0.01 and p < 0.05, respectively) and nitric oxide (NO) production had increased at 4 hours as shown by NADPH diaphorase staining. In the IL-18+endotoxin group, the decrement of the force-frequency curves in a higher frequency range (50-120 Hz), and the decrements of TT and TT/CT observed at 4 hours in the saline+endotoxin group were significantly prevented, and NO production was blocked at 4 hours. In the IL-18 only group, the force-frequency curves did not change except for fatigability, and NO production did not occur. It is suggested that IL-18 itself naturally blocks NO production, even when endotoxin coexists, resulting in the prevention of deterioration of diaphragm muscle contraction by endotoxin.

Animals↗
PubMedDate not supplied

Signal transduction in esophageal and LES circular muscle contraction.

Contraction of normal esophageal circular muscle (ESO) in response to acetylcholine (ACh) is linked to M2 muscarinic receptors activating at least three intracellular phospholipases, i.e., phosphatidylcholine-specific phospholipase C (PC-PLC), phospholipase D (PLD), and the high molecular weight (85 kDa) cytosolic phospholipase A2 (cPLA2) to induce phosphatidylcholine (PC) metabolism, production of diacylglycerol (DAG) and arachidonic acid (AA), resulting in activation of a protein kinase C (PKC)-dependent pathway. In contrast, lower esophageal sphincter (LES) contraction induced by maximally effective doses of ACh is mediated by muscarinic M3 receptors, linked to pertussis toxin-insensitive GTP-binding proteins of the G(q/11) type. They activate phospholipase C, which hydrolyzes phosphatidylinositol bisphosphate (PIP2), producing inositol 1,4,5-trisphosphate (IP3) and DAG. IP3 causes release of intracellular Ca++ and formation of a Ca++-calmodulin complex, resulting in activation of myosin light chain kinase and contraction through a calmodulin-dependent pathway. Signal transduction pathways responsible for maintenance of LES tone are quite distinct from those activated during contraction in response to maximally effective doses of agonists (e.g., ACh). Resting LES tone is associated with activity of a low molecular weight (approximately 14 kDa) pancreatic-like (group 1) secreted phospholipase A2 (sPLA2) and production of arachidonic acid (AA), which is metabolized to prostaglandins and thromboxanes. These AA metabolites act on receptors linked to G-proteins to induce activation of PI- and PC-specific phospholipases, and production of second messengers. Resting LES tone is associated with submaximal PI hydrolysis resulting in submaximal levels of inositol trisphosphate (IP3-induced Ca++ release, and interaction with DAG to activate PKC. In an animal model of acute esophagitis, acid-induced inflammation alters the contractile pathway of ESO and LES. In LES circular muscle, after induction of experimental esophagitis, basal levels of PI hydrolysis are substantially reduced and intracellular Ca++ stores are functionally damaged, resulting in a reduction of resting tone. The reduction in intracellular Ca++ release causes a switch in the signal transduction pathway mediating contraction in response to ACh. In the normal LES, ACh causes release of Ca++ from intracellular stores and activation of a calmodulin-dependent pathway. After esophagitis, ACh-induced contraction depends on influx of extracellular Ca++, which is insufficient to activate calmodulin, and contraction is mediated by a PKC-dependent pathway. These changes are reproduced in normal LES cells by thapsigargin-induced depletion of Ca++ stores, suggesting that the amount of Ca++ available for release from intracellular stores defines the signal transduction pathway activated by a maximally effective dose of ACh.

Acetylcholine↗
PubMed1980

Effects of deuterium oxide on mechanics and energetics of skeletal muscle contraction.

Mechanics and energetics of contraction were studied in isolated frog semitendinosus muscles (n = 15) in deuterium oxide (D2O) at 5 degrees C. Twitch force and energy liberation (heat + work) in 99.8% D2O-Ringer at lo were 4 +/- 0.8 and 22 +/- 1%, respectively, of control values. Tetanus force was slowed in development, and developed tetanus force was reduced to 89 +/- 7% of control values. With repeated tetanic contractions, the rate of force development increased, and peak force increased above control values in some muscles. The twitch was potentiated 10-fold (10 +/- 2) after repeated tetanic contractions. Energy liberation increased but not in proportion to force. Ca2+ cycling energy liberation or activation heat, estimated from stretched muscles, was 60 +/- 3% of control values. With maximum posttetanic twitch potentiation, the activation heat increased by 25 +/- 3%. Peak twitch force and energy liberation occurred at longer muscle lengths than in normal Ringer. After correcting for small differences in force development at lo and 1.38 +/- 0.01 lo, it was possible to estimate the effect of length per se on energy liberation. Under these conditions, there was an 8 +/- 2% decrease in energy liberation at 1.38 lo.

Action Potentials↗
PubMed1992

Direct effects and augmentation of airway smooth muscle contraction caused by phospholipase A2.

We examined the effect of phospholipase A2 (PLA2; Naja naja) on isometric tracheal smooth muscle force generation in guinea pig trachealis in situ. Direct application of PLA2 to the surface of the trachea caused dose-related contraction of tracheal smooth muscle. In seven guinea pigs, a dose/density of 100 micrograms/cm2 PLA2 caused active tension (AT) that began immediately and was maximum (1.32 +/- 0.13 g/cm) at 5 min (p less than 0.01 versus baseline tension). PLA2 also augmented the contractile response to intravenously administered acetylcholine (ACh); AT caused by 3 x 10(-7) mol/kg ACh was 0.98 +/- 0.13 g/cm after PLA2 versus 0.64 +/- 0.09 g/cm in control animals (p = 0.003). PLA2 inactivated with bromophenacyl bromide (BPB) prior to topical application neither caused contraction (-0.18 +/- 0.18 g/cm AT, p = NS versus baseline tension) nor altered muscarinic responsiveness to 3 x 10(-7) mol/kg ACh. Contraction caused by 100 micrograms/cm2 PLA2 was greater after epithelium removal (2.73 +/- 0.40 g/cm AT versus 1.32 +/- 0.13 g/cm AT in epithelium-intact animals, p less than 0.005). However, epithelium removal (confirmed histologically) attenuated completely augmentation of muscarinic contraction caused by PLA2. Augmentation of muscarinic contraction also was blocked with 15 mg/kg 3-amino-1-(3-trifluoromethylphenyl)-2-pyrazoline hydrochloride (BW 755c), an inhibitor of eicosanoid synthesis, administered intravenously 30 min prior to topical application of 100 micrograms/cm2 PLA2. In contrast, contraction of tracheal smooth muscle caused by PLA2 was not affected significantly by blockade of eicosanoid synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2003

Role of Crk-associated substrate in the regulation of vascular smooth muscle contraction.

A pool of actin monomers is induced to polymerize into actin filaments during contractile stimulation of smooth muscle. The inhibition of actin dynamics by actin polymerization inhibitors depresses active force generation in smooth muscle. In this study, we hypothesized that Crk-associated substrate plays a role in the regulation of contraction and actin dynamics in vascular smooth muscle. Antisense or sense oligodeoxynucleotides for Crk-associated substrate were introduced into carotid smooth muscle tissues by chemical loading. The treatment of smooth muscle strips with antisense oligodeoxynucleotides inhibited the expression of Crk-associated substrates; it did not influence the expression of actin, myosin heavy chain, and paxillin. Sense oligodeoxynucleotides did not affect the expression of these proteins in smooth muscle tissues. Force generation in response to stimulation with norepinephrine or KCl was significantly lower in antisense-treated muscle strips than in sense-treated strips or in muscle strips not treated with oligodeoxynucleotides. The downregulation of Crk-associated substrate did not attenuate increases in phosphorylation of the 20-kDa regulatory light chain of myosin in response to stimulation with norepinephrine. The increase in F-actin/G-actin ratio during contractile stimulation was significantly inhibited in antisense-treated smooth muscle strips. Contractile activation of smooth muscle increased the association of profilin with actin monomers; the depletion of Crk-associated substrate inhibited the increases in the profilin-actin complex in response to contractile stimulation. These results suggest that Crk-associated substrate is a necessary molecule of signaling cascades that regulate active force generation in smooth muscle. This molecule may regulate actin dynamics in smooth muscle in response to contractile stimulation.

Actins↗
PubMed1998

ATP analogs and muscle contraction: mechanics and kinetics of nucleoside triphosphate binding and hydrolysis.

The mechanical behavior of skinned rabbit psoas muscle fiber contractions and in vitro motility of F-actin (Vf) have been examined using ATP, CTP, UTP, or their 2-deoxy forms (collectively designated as nucleotide triphosphates or NTPs) as contractile substrates. Measurements of actin-activated heavy meromyosin (HMM) NTPase, the rates of NTP binding to myosin and actomyosin, NTP-mediated acto-HMM dissociation, and NTP hydrolysis by acto-HMM were made for comparison to the mechanical results. The data suggest a very similar mechanism of acto-HMM NTP hydrolysis. Whereas all NTPs studied support force production and stiffness that vary by a factor 2 or less, the unloaded shortening velocity (Vu) of muscle fibers varies by almost 10-fold. 2-Deoxy ATP (dATP) was unique in that Vu was 30% greater than with ATP. Parallel behavior was observed between Vf and the steady-state maximum actin-activated HMM ATPase rate. Further comparisons suggest that the variation in force correlates with the rate and equilibrium constant for NTP cleavage; the variations in Vu or Vf are related to the rate of cross-bridge dissociation caused by NTP binding or to the rate(s) of product release.

Acid Anhydride Hydrolases↗
PubMed1990

Influence of temperature on mechanics and energetics of muscle contraction.

Results gleaned from use of temperature as a probe to study skeletal muscle performance and mechanisms of activation and contraction are reviewed. Steady-state and non-steady-state responses to changes in temperature are considered. Temperature sensitivities, Q10 values, of mechanical and energetic parameters range from nearly 1 to greater than 5 in frog skeletal muscle. Factors that are less temperature sensitive (Q10 less than or equal to 1.5) are peak tetanic force, instantaneous stiffness, curvature of force-velocity relation, magnitude of labile heat, and mechanical efficiency. Rates with intermediate temperature sensitivities (Q10 greater than 2 but less than 3) include rate of isometric force development, maximum shortening velocity, and relaxation from a brief tetanus. Rates with high temperature sensitivities (Q10 greater than 3) include cross-bridge turnover during an isometric tetanus, isometric economy, maximum power output, Ca2+ sequestration by sarcoplasmic reticulum, relaxation from a prolonged tetanus, and recovery metabolism. The observation that the Q10 for relaxation rate depends on tetanic duration can be explained in terms of the possible role of parvalbumin as a soluble relaxing factor.

Animals↗
PubMed1993

NMR and analytic biochemical evaluation of CrP and nucleotides in the human calf during muscle contraction.

This study compared biochemical and 31P-nuclear magnetic resonance (NMR) determinations of energy metabolites during isometric contractions of the human calf muscle at various exercise intensities. Seven male subjects performed one-legged isometric contractions at a work load of 28, 64, and 90% of maximal voluntary contraction force (28-, 64-, and 90%-CON, respectively) for 3 min, 40 s, and 40 s, respectively, in a magnet and in an exact model of the magnet with an arrangement for rapid muscle biopsy sampling from the gastrocnemius. The decrease in phosphocreatine (CrP) determined by NMR was 20, 33, and 71% for 28%-, 64%-, and 90%-CON, respectively. These decreases were the same as those determined biochemically (25, 34, and 61%, respectively). Muscle CrP 1 min after 90%-CON was also found to be similar between NMR and biochemical determinations (88 and 74% of resting value, respectively). Although no significant change in muscle ATP was found by NMR, a decrease of 29% was observed biochemically at 90%-CON. The ratio between muscle CrP and ATP was the same between NMR and biochemical determinations except for 90%-CON (1.98 and 0.78, respectively). The increase in muscle ADP determined by NMR was two-, five-, and eightfold higher than that found biochemically for 28%-, 64%-, and 90%-CON, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

[Effects of fatigue on the characteristics of cat gastrocnemius muscle contraction and elongation in response to changes of the controlled load].

Spreading of fatigue-related effects from active to inactive parts in the cat gastrocnemius muscle was studied. Fatiguing contractions of a part of gastrocnemius muscle were evoked through stimulation of the cut ventral root (VR) S1 with rate 50 s(-1) during 20 s followed by 10 s of rest, over 10-30 min (CFS). To test activation of a non-active part of this muscle the distributed stimulation of dissected VR L7 with rate of 10 s(-1) per filament was applied. After achieving by the muscle a steady-state level of isometric contraction, a quick transition to isotonic condition was produced. Transient responses of shortening and lengthening were analyzed in terms of the two-component model including the fast inertialess and slow aperiodic components. Test duration was 12 s, time intervals between tests consisted of 3 min. CFS reduced isometric force of the tested part of muscle as well as the velocity of shortening and lengthening. The muscle lengthening had been slowing down with development of the fatigue effects; the final steady value of the muscle length in transients was reduced, while weight of the inertialess component increased. Slowing of shortening was accompanied by reduction of the final length amplitude and the time constants of aperiodic component were increased. We suppose that diffusion of metabolites from active to inactive muscle fibers was the major reason for contractility deterioration.

Animals↗
PubMed1990

The augmenting action of banana tree juice on skeletal muscle contraction.

An extract obtained from juice expressed from the stem of the plantain banana tree (Musa sapientum L., var. paradisiaca) induces twitch augmentation in skeletal muscles. The mechanism of this action was investigated in the mouse hemi-diaphragm preparation. Directly evoked twitches and potassium induced (K+) contractures were both augmented by the extract. Twitch augmentation was partly dependent on extracellular Ca2+. The action on K(+)-contractures was unaffected by tetrodotoxin, but the rate of relaxation was enhanced in the absence of extracellular calcium (0[Ca2+]o). Muscle contracture induced by high concentrations of extract was also augmented in 0[Ca2+]o and in the presence of the Ca2(+)-channel blocking agent, nifedipine. The time course of the contracture was shortened in 0[Ca2+]o, but not by nifedipine. Nifedipine enhanced the augmenting effect of the extract on twitches but shortened the time-course of this action. In addition, a muscle contracture was superimposed on the twitching muscle at higher concentrations of nifedipine. Manganese, on the other hand, reduced or abolished the augmenting action of the extract. The results are consistent with an action of banana tree juice on the molecule responsible for excitation-contraction coupling in skeletal muscle, resulting in a labilization of intracellular Ca2+.

Animals↗
PubMed2006

Insulin induces airway smooth muscle contraction.

BACKGROUND AND PURPOSE: Recently, the use of inhaled insulin formulations for the treatment of type I and type II diabetes has been approved in Europe and in the United States. For regular use, it is critical that airway function remains unimpaired in response to insulin exposure. EXPERIMENTAL APPROACH: We investigated the effects of insulin on airway smooth muscle (ASM) contraction and contractile prostaglandin (PG) production, using guinea-pig open-ring tracheal smooth muscle preparations. KEY RESULTS: It was found that insulin (1 nM-1 microM) induced a concentration-dependent contraction that was insensitive to epithelium removal. These sustained contractions were susceptible to inhibitors of cyclooxygenase (indomethacin, 3 microM), Rho-kinase (Y-27632, 1 microM) and p42/44 MAP kinase (PD-98059, 30 microM and U-0126, 3 microM), but not of PI-3-kinase (LY-294002,10 microM). In addition, insulin significantly increased PGF(2alpha)-production which was inhibited by indomethacin, but not Y-27632. Moreover, the FP-receptor antagonist AL-8810 (10 microM) and the EP(1)-receptor antagonist AH-6809 (10 microM) strongly reduced insulin-induced contractions, supporting a pivotal role for contractile prostaglandins. CONCLUSIONS AND IMPLICATIONS: Collectively, the results show that insulin induces guinea-pig ASM contraction presumably through the production of contractile prostaglandins, which in turn are dependent on Rho-kinase for their contractile effects. The data suggest that administration of insulin as an aerosol could result in some acute adverse effects on ASM function.

Animals↗
PubMed1983

Invariance of ankle dynamic stiffness during fatiguing muscle contractions.

Our objective was to determine the effect of muscle fatigue on the dynamic stiffness of the human ankle. Four subjects were required to maintain constant-force contractions of tibialis anterior until the required force could no longer be maintained. Repeated pseudo-random displacements of ankle angular position were applied throughout each contraction. The dynamic relation between ankle angular position and ankle torque was identified by determining non-parametric compliance impulse response functions (CIRFs). The CIRFs were redetermined every 2.55S throughout the sustained contractions to provide a quantitative measure of changes in ankle stiffness dynamics. Inspection of these CIRFS revealed little change in shape or magnitude throughout the contractions, despite large increases in tibialis anterior EMG. The dynamics were further quantified by estimating the equivalent joint inertia, viscosity and elasticity associated with each CIRF. As each contraction progressed, the inertial and elastic terms remained constant whereas the viscous term decreased slightly. These findings demonstrate that fatigue of tibialis anterior during sustained constant mean force contractions results in little change in the mechanical dynamics of the human ankle.

Adult↗
PubMed2002

Energy consumption in static muscle contraction.

Energy consumption during static contraction of the human triceps surae muscles was studied in 11 healthy subjects. The subjects had to stand intermittently on the left and then right foot at different frequencies (for periods of 15 s, 10 s or 5 s), first on the whole foot and then on the forefoot. The mean static energy consumption of all subjects was 13.4 (15) W [mean (s.d.)] at a calf muscle moment of 105 Nm. Assuming that static energy consumption (in W) is proportional to static moment (in Nm), a proportionality factor of 0.17 (0.19) s(-1) is found. Because of the limited attainable accuracy, no significant differences between endurance athletes and sprinters could be found.

Adult↗
PubMed1977

Effect of dantrolene sodium on muscle contraction.

The force of contraction of the adductor pollicis before and after dantrolene sodium was evaluated in 5 paraplegic patients. The muscle was indirectly stimulated through supramaximal stimulation of the ulnar nerve at the wrist, with single pulse and variable number of stimuli at frequency of 50 Hz. There was a marked and significant reduction (an average of 64%) of the single twitch response in all patients while on medication. When the muscle, however, was stimulated with tetanic frequency no significant difference was evident in the force of the sustained contraction with or without medication. The amplitude of evoked electrical potentials, simultaneously recorded from the adductor pollicis remained unchanged irrespective of the status of medication. Decrement of the twitch response, with no effect on the electrical activity, tends to substantiate the distal effects of dantrolene on muscle contraction. The drug, however, does not seem to prevent the muscle from achieving its normal maximal tetanic force when activated with frequencies close to the physiological frequencies of maximal, voluntary effort (50 Hz.) These effects point to the usefulness and limitations of the drug in clinical situations.

Adolescent↗
PubMed1976

[The pressor reflex induced by skeletal muscle contraction and its influence on the reflex from the sino-aortic zones].

The cardiovascular response to 10 sec tetanic muscular contractions was studied in the decerebrated cat. A pressor reflex about 30 mm Hg occurred during hindlimb contractions evoked by ventral roots (L6, L7, S1) stimulation. The pressor reflex was associated with a decrease of blood flow in working and resting muscles and a minimal changes of heart rate and left ventricular contractility. An increase of systemic resistance, as a main cause of pressor reflex is suggested. Static contractions of muscles and stimulation of muscle nerve evoked stronger inhibition of baroreflex than cutaneous nerve stimulation of nociceptive stimuli. Inhibition of the cardiac component of baroreflex during muscular exercise was shown.

Animals↗
PubMed1998

Alpha1L-adrenoceptor mediation of smooth muscle contraction in rabbit bladder neck: a model for lower urinary tract tissues of man.

1. The alpha1-adrenoceptor population mediating contractile responses to noradrenaline (NA) in smooth muscles of the bladder neck from rabbit (RBN) has been characterized by use of quantitative receptor pharmacology. 2. Experiments with several 'key' alpha1-adrenoceptor antagonists of varying subtype selectivities (RS-17053, BMY 7378, indoramin, 5-methylurapidil, prazosin, REC 15/2739, SNAP 5089, terazosin, WB 4101, tamsulosin, (+)-cyclazosin and RS-100329) were conducted. Schild regression analyses yielded affinity (mean pKb) estimates of 7.1, 6.2, 8.6, 8.6, 8.4, 9.3, 7.0, 7.4, 8.9, 10.0, 7.1 and 9.3, respectively, although deviations from unit Schild regression slope question the robustness of data for RS-17053 and SNAP 5089. 3. The nature of antagonism by these agents and the profile of affinity determinations generated together suggest that a single alpha1-adrenoceptor subtype mediates contractile responses of RBN to NA. Additional studies with phenylephrine indicated also an agonist-independence of this profile. Pharmacologically, this profile was reminiscent of that described as 'alpha1L'-adrenoceptor, which has been shown to mediate contractions of several tissues including lower urinary tract (LUT) tissues of man. Furthermore, a similarity was noticed between the 'alpha1L'-adrenoceptor described here in RBN and the rabbit and human cloned alpha1a-adrenoceptor (based on data from both whole cell radioligand binding at 37 degrees C and [3H]-inositol phosphates accumulation assays), characterizations of which have been published elsewhere. 4. In conclusion, the RBN appears to provide a predictive pharmacological assay for the study of NA-induced smooth muscle contraction in LUT tissues of man.

Adrenergic alpha-1 Receptor Antagonists↗