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 1,459 records · Page 81Linked to original sources
PubMed1996

Human motor unit activity during post-vibratory and imitative voluntary muscle contractions.

Applying mechanical vibration for short periods to a muscle tendon induces long-lasting involuntary contractions which develop soon after the vibration offset in the previously vibrated muscle. In the present study, the question was raised as to whether these post-vibratory motor responses are mediated by the activity of supraspinal neural population or whether they may involve in addition some peripheral facilitatory influences operating at the motoneuronal level. To investigate this question, we analysed the unitary activity of 48 motor units belonging to the wrist extensor radialis muscles of the human hand, after attempting to classify them as slow or fast, during both post-vibratory and voluntary contractions having almost the same amplitudes and time-courses. The motor units were found to be activated in much the same way with both types of contraction. Similarities were observed as regards: the nature of the motor units activated, the order of recruitment of the motor unit population, the motor units' force recruitment thresholds, the mean interspike interval and the standard deviation. These analogies suggest that post-vibratory contraction may mainly involve a supraspinal tonic drive, but the possibility that these involuntary contractions may have a spinal origin cannot be completely ruled out.

Action Potentials↗
PubMed1992

Effects of cricothyroid muscle contraction on upper airway flow dynamics in dogs.

We studied the effects of cricothyroid muscle (CT) contraction on upper airway flow dynamics in eight prone open-mouth anesthetized dogs. Animals were mechanically ventilated via a tracheostomy while a constant airflow (Vuaw) passed through the isolated upper airway. Nasal airflow (Vn) was monitored using a nasal mask and pneumotachograph. Bilateral CT contraction was induced by electrical stimulation of the external branches of the superior laryngeal nerves. During CT contraction with Vuaw of 100-443 ml/s in the inspiratory direction, total upper airway resistance (Ruaw) fell by 49.1 +/- 5.4% (SE) while supraglottic resistance fell by 63.6 +/- 3.6%; simultaneously Vn fell by 55.3 +/- 3.8% and Vuaw increased by 7.2 +/- 1.7%. Similar results were obtained when Vuaw was in the expiratory direction. In three dogs in which the attachments of the CT to either the thyroid or cricoid cartilage were severed, superior laryngeal nerve stimulation had no systematic effect on Ruaw. Because visual assessment during CT contraction consistently revealed dilation of the piriform recesses, we suggest that CT contraction is associated with pharyngeal dilation, which in open-mouth dogs (with overlapping soft palate and epiglottis) redistributes flow to the oral route with a net reduction in Ruaw. Thus the CT may have a respiratory role as a pharyngeal dilator.

Airway Resistance↗
PubMed1992

Partial inhibition of skeletal muscle contraction by dantrolene sodium and its modification with perchlorate and Bay K 8644.

The effects of dantrolene sodium (DAN) on the dihydropyridine receptor (DHPR) of the transverse (T) tubule voltage sensor (Ca2+ channel) was studied with single fibers from bullfrog toe muscle. Perchlorate (ClO4-), which acts selectively on the DHPR, overcame DAN-induced inhibition of twitch tension. Bay K 8644, a DHPR agonist, slowed the rate of twitch inhibition by DAN. DAN inhibited twitch tension to a greater extent in Ca(2+)-free solution than in Ringer solution or solution containing Zn2+, whereas twitch inhibition by DAN was less in caffeine-containing solution than in the control. The effects of DAN on Zn(2+)- and caffeine-treated fibers and on fibers in Ca(2+)-free solution suggest that DAN must act near the voltage sensor of the T tubule. However, differences in net twitch inhibition by DAN between control fibers and fibers potentiated by ClO4- or Bay K 8644 suggest that DAN does not bind to the same site as these potentiating agents do. The role of myoplasmic Ca2+ in DAN-induced inhibition of twitch and the effects of DAN on the mechanical threshold and membrane potential in skeletal muscle are discussed.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1980

[Mechanisms of activation of coronary vessel smooth muscle contraction].

Experiments have been performed with smooth muscle cells (SMC) of the circular strips from the bovine left descending anterior heart artery with a diameter of 2--2.5 mm. Use was made of the double sucrose gap method with simultaneous recording of electric and contractile activity of SMC. The cathode of polarizing current produced depolarization of SMC membrane (cathelectrotone). After depolarization of the membrane reached the threshold, the action potential (AP) was generated, followed by SMC contraction. The anode of polarizing current caused hyperpolarization of the membrane (anelectrotone) accompanied by relaxation of the strip. The degree of relaxation depended upon the initial muscle tone and the magnitude of anelectrotonic hyperpolarization. The voltage-current characteristics of SMC show that the muscle cell membrane of the coronary arteries possesses pronounced rectifying properties. An increase in the external potassium concentration up to 160 mM results in depolarization of the SMC membrane preceded by AP. These changes are accompanied by initial phasic and subsequent tonic contraction. The phasic component of the contraction is suggested to be evoked by AP and tonic component by stable potassium depolarization.

Action Potentials↗
PubMed1998

Insulin inhibits vascular smooth muscle contraction at a site distal to intracellular Ca2+ concentration.

Several hypertensive states are associated with resistance to insulin-induced glucose disposal and insulin-induced vasodilation. Insulin can inhibit vascular smooth muscle (VSM) contraction at the level of the VSM cell, and resistance to insulin's inhibition of VSM cell contraction may be of pathophysiological importance. To understand the VSM cellular mechanisms by which insulin resistance leads to increased VSM contraction, we sought to determine how insulin inhibits contraction of normal VSM. It has been shown that insulin lowers the contractile agonist-stimulated intracellular Ca2+ (Ca2+i) transient in VSM cells. In this study, our goal was to see whether insulin inhibits VSM cell contraction at steps distal to Ca2+i and, if so, to determine whether the mechanism is dependent on nitric oxide synthase (NOS) and cGMP. Primary cultured VSM cells from canine femoral artery were bathed in a physiological concentration of extracellular Ca2+ and permeabilized to Ca2+ with a Ca2+ ionophore, either ionomycin or A-23187. The resultant increase in Ca2+i contracted individual cells, as measured by photomicroscopy. Preincubating cells with 1 nM insulin for 30 min did not affect basal Ca2+i or the ionomycin-induced increase in Ca2+i, as determined by fura 2 fluorescence measurements, but it did inhibit ionomycin- and A-23187-induced contractions by 47 and 51%, respectively (both P < 0.05). In the presence of 1.0 microM ionized Ca2+, ionomycin-induced contractions were inhibited by insulin in a dose-dependent manner. In the presence of ionomycin, insulin increased cGMP production by 43% (P < 0.05). 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10 microM), a selective inhibitor of guanylate cyclase that blocked cGMP production in these cells, completely blocked the inhibition by insulin of ionomycin-induced contraction. It was found that the cells expressed the inducible isoform of NOS. NG-monomethyl-L-arginine or NG-nitro-L-arginine methyl ester (0.1 mM), inhibitors of NOS, did not affect ionomycin-induced contraction but prevented insulin from inhibiting contraction. We conclude that insulin stimulates cGMP production and inhibits VSM contraction in the presence of elevated Ca2+i. This inhibition by insulin of VSM contraction at sites where Ca2+i could not be rate limiting is dependent on NOS and cGMP.

Animals↗
PubMed1994

Path and extent of cross-bridge rotation during muscle contraction.

The angular distribution of myosin cross-bridges in muscle fibers was investigated in four physiological states using a multiple probe analysis of varied extrinsic probes of the cross-bridge [Burghardt & Ajtai (1994) Biochemistry (preceding paper in this issue)]. The analysis combines data of complementary techniques from different probes giving the highest possible angular resolution. Four extrinsic probes of the fast reactive sulfhydryl (SH1) on myosin subfragment 1 (S1) were employed. Electron paramagnetic resonance (EPR) spectra from paramagnetic probes, deuterium- and 15N-substituted for greater sensitivity to orientation, on S1 were measured when the protein was freely tumbling in solution and when it was decorating muscle fibers. The EPR spectra from labeled S1 tumbling in solution were measured at X- and Q-band microwave frequencies to uniquely specify the orientation of the probe relative to the S1 principal hydrodynamic frame. The EPR spectra from labeled S1 decorating muscle fibers in rigor and in the presence of MgADP were measured at X-band and used in the multiple probe analysis of cross-bridge orientation. The time-resolved fluorescence anisotropy decay (TRFAD) of fluorescent probes on S1 was measured when the protein was freely tumbling in solution, and fluorescence polarization (FP) intensities from fluorescent probes modifying SH1 in intact muscle fibers were measured for fibers in rigor, in the presence of MgADP, in isometric contraction, and in relaxation at low ionic strength. The TRFAD measurements limit the range of possible orientations of the probe relative to the S1 principal hydrodynamic frame. The FP intensity measurements were used in the multiple probe analysis of cross-bridge orientation. The combination of the EPR and FP data determined a highly resolved cross-bridge angular distribution in rigor, in the presence of MgADP, in isometric contraction, and in relaxation at low ionic strength. These findings confirm earlier observations of a rigid body rotation of the SH1 region in the myosin head group upon physiological state changes and indicate the path and extent of cross-bridge rotation during contraction. The rotation of the cross-bridge is visualized with computer-generated space-filling models of actomysin in six states of the contraction cycle.

Adenosine Diphosphate↗
PubMed2003

Effects of chloroquine on smooth muscle contracted with noradrenaline or high-potassium solutions in the rat thoracic aorta.

The effects of chloroquine on the smooth muscle of isolated rat aortic segments were investigated in preparations contracted with either noradrenaline or high-potassium. At rest, chloroquine (up to 10(-4) M) produced no mechanical response, while noradrenaline (10(-6) M) produced a sustained contraction. In the presence of 10(-4) M chloroquine, however, the amplitude of contractions produced by noradrenaline was attenuated by about 70%, with no alteration of the resting tension. In preparations contracted either with noradrenaline or with high-K solutions, chloroquine produced a concentration-dependent relaxation. The tension decreased below resting level as a result of the co-application of these stimulants. The relaxing actions of chloroquine were not altered by methylene blue (an inhibitor of guanylate cyclase), suggesting that the cyclic GMP-related mechanism was not involved. The ratio of the amplitude of chloroquine-induced relaxation was similar in contractions produced by different concentrations of potassium ions, suggesting that chloroquine did not cause relaxation as a result of membrane hyperpolarization. These results suggest that the inhibition of aortic smooth muscle contraction caused by chloroquine is different to that produced by endothelium-derived vasodilating factors. It is possible that the inhibition of aortic smooth muscle contraction by chloroquine involves modulation of the contractile systems and of their regulatory proteins.

Animals↗
PubMed1997

Blockade of nitric oxide-evoked smooth muscle contractions by an inhibitor of guanylyl cyclase.

Nitric oxide-induced contractile responses of smooth muscle were studied in vitro in guinea-pig small intestine. Application of nitric oxide (NO; 0.3-30 microM) evoked a small initial relaxation followed by a marked contractile response in plexus-containing longitudinal smooth muscle preparations from small intestine. The extent of the NO-evoked contractile response was dose-dependent and the response was blocked by tetrodotoxin. Atropine significantly reduced the NO-evoked contraction and the remaining part was abolished by the NK1-receptor antagonist CP 96,345. An inhibitor of soluble guanylyl cyclase, ODQ (1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one), abolished the NO-evoked contractile response. The results suggest that NO, in addition to the classical direct smooth muscle relaxing effect, causes activation of excitatory neurones, via a pathway utilizing soluble guanylyl cyclase, which leads to a smooth muscle contraction.

Animals↗
PubMed1993

Dystrophin protects the sarcolemma from stresses developed during muscle contraction.

The protein dystrophin, normally found on the cytoplasmic surface of skeletal muscle cell membranes, is absent in patients with Duchenne muscular dystrophy as well as mdx (X-linked muscular dystrophy) mice. Although its primary structure has been determined, the precise functional role of dystrophin remains the subject of speculation. In the present study, we demonstrate that dystrophin-deficient muscle fibers of the mdx mouse exhibit an increased susceptibility to contraction-induced sarcolemmal rupture. The level of sarcolemmal damage is directly correlated with the magnitude of mechanical stress placed upon the membrane during contraction rather than the number of activations of the muscle. These findings strongly support the proposition that the primary function of dystrophin is to provide mechanical reinforcement to the sarcolemma and thereby protect it from the membrane stresses developed during muscle contraction. Furthermore, the methodology used in this study should prove useful in assessing the efficacy of dystrophin gene therapy in the mdx mouse.

Animals↗
PubMed1994

Schistosoma mansoni: myogenic characteristics of phorbol ester-induced muscle contraction.

The myogenic nature of phorbol ester-induced muscle contractures of Schistosoma mansoni was investigated using muscle physiology and electrophysiological techniques. The contracture is dependent of extracellular Ca2+, is blocked by Ca2+ channel blockers, and appears to be associated with an increase in the permeability of the muscle to Ca2+ but not to Na+ or H+. The musculature is not depolarized during phorbol ester-induced contracture, but surface electrical activity decreases. Threshold treatments of phorbol ester and depolarization or praziquantel produce synergistic contractures of the parasite. The contracture could not be explained by altered release of or sensitivity to putative neurotransmitters, decreased Ca2+ efflux, or an increase in the sensitivity of the contractile system to Ca2+. These results support the hypothesis that activation of protein kinase-C in the schistosome with phorbol esters leads to muscle contracture by enhancing sarcolemmal Ca2+ channel activity.

Acetylcholine↗