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PubMedDate not supplied

[Effect of sydnophen and caffeine on reflex shifts in arterial pressure arising during skeletal muscle contraction].

The influence of sydnophen (5-20 mg/kg) and of caffein (10-40 mg/kg) on the pressor reaction of the arterial pressure, provoked by contraction of skeletal muscles following stimulation of the anterior spinal cord roots (L6, L7, S1) was investigated in 17 tests set up on decerebrated non-narcotized cats. The intraveonus injection of sydnophen was attended by a fall of the arterial pressure and inhibition of the pressor reflex. Caffein reduced the intensity of the pressor reflex to a lesser extent and did not modify the initial level of the arterial pressure.

Animals↗

PubMed1996

Electrostatic forces as a possible mechanism underlying skeletal muscle contraction.

A possible mechanism is put forward to explain the sliding of thin filaments during muscle contraction. In our model, repulsion due to electrostatic forces is the mechanism which triggers crossbridges to cause the thin filaments to slide. The mechanism proposed could operate regardless of whether the myosin heads rotate or bend, although recent experimental evidence seems to confirm the latter action. In spite of its simplicity, the model prediction of the velocity of sliding of the thin filaments agrees well with experimental values from in vitro motility assays.

Actins↗

PubMed2006

Tachykinins are involved in local reflex modulation of vagally mediated striated muscle contractions in the rat esophagus via tachykinin NK1 receptors.

The objective of the present study was to investigate the hypothesis of the presence of a local neural reflex modulating the vagally mediated contractions of striated muscle in the rat esophagus and to determine the possible involvement of tachykinins in such a local neural reflex. Electrical stimulation of the vagus nerve evoked twitch contractile responses that were abolished by d-tubocurarine (5 microM). Capsaicin (1-100 microM) inhibited the vagally mediated twitch contractions o f the normal rat esophageal preparations concentration-dependently but not those of the neonatally capsaicin-treated ones. NG-nitro-L-arginine methyl ester (100 microM), a nitric oxide synthase inhibitor, blocked the inhibitory effect of capsaicin and exogenous application of a nitric oxide donor (1 mM) inhibited the vagally mediated twitch contractions. Capsaicin suppressed acetylcholine release from the normal rat esophageal segments evoked by vagus nerve stimulation but not that from the neonatally capsaicin-treated ones. A selective tachykinin NK1 receptor antagonist (0.1 or 1 microM) attenuated the inhibitory effect of capsaicin. However, antagonists of tachykinin NK2, tachykinin NK3 and calcitonin gene-related peptide receptors (1 microM) did not have any effect. A tachykinin NK1 receptor agonist (1 or 5 microM) inhibited the vagally mediated twitch contractions, which was prevented by NG-nitro-L-arginine methyl ester (100 microM). These data suggest that the rat esophagus might have a local neural reflex inhibiting the vagally mediated striated muscle motility, which consists of capsaicin-sensitive sensory neurons and myenteric nitrergic neurons, and that tachykinins might be involved in the neural reflex through tachykinin NK1 receptors.

Acetylcholine↗

PubMed1988

Muscle contraction and movement of cellular organelles: are there two different types of mechanisms for their generation?

It has been shown that myosin molecules attached to Covaspheres can "walk along" polar actin filament in vitro. The driving force for this movement seems to explain only about 1% of the isometric tension developed by a muscle fibre. Therefore, the driving force for the bead movement seems to be incompatible with that found in muscle, and the bead movement cannot be considered as a model for muscle contraction. The origin of the bead movement may be related to a "molecular jet" process, resulting from the rapid ejection of the MgATP splitting products. This "molecular jet" might also explain the movements of many cellular organelles.

Actins↗

PubMed1996

Prostate specific antigen releases a kinin-like substance on proteolysis of seminal vesicle fluid that stimulates smooth muscle contraction.

PURPOSE: We investigated whether purified prostate specific antigen (PSA), a seminal plasma serine protease of the kallikrein enzyme family, is capable of releasing kinin-like peptides from natural substrate glycoproteins in human seminal vesicle fluid. MATERIALS AND METHODS: An in vivo rat bladder model was used to monitor for release of substances capable of inducing smooth muscle contractions. Purified PSA, seminal vesicle fluid (SVF) from radical prostatectomy specimens, bradykinin, saline and a bradykinin antagonist were injected intravesically into urethane-anesthetized rats, and the resulting bladder contractions were measured. RESULTS: Injection of either PSA or SVF alone did not induce bladder contractions. Injection of a mixture of SVF and PSA preincubated 15 minutes, however, induced strong bladder contractions (23 +/- 7 cm. H2O) that decreased with time (4 +/- 2 cm. H2O, after 90 minutes). Similar contractions were observed after injection of bradykinin (10(-4) M. = 39 +/- 14, 10(-6) M. = 27 +/- 9, 10(-8) M. = 7 +/- 4 cm. H2O). Addition of a bradykinin antagonist to the PSA-SVF mixture prior to injection blocked the observed bladder contractions (23 +/- 7 cm. H2O before, versus 0.3 +/- 1.2 cm. H2O after adding antagonist). CONCLUSIONS: We conclude that PSA produces a kinin-like substance by enzymatic cleavage of glycoproteins in human seminal fluid. This substance induces smooth muscle contractions which can be specifically blocked by addition of a bradykinin antagonist.

Animals↗

PubMed1981

Magnesium and the regulation of muscle contraction.

There are a variety of Ca2+ binding sites in muscle (e.g., troponin, parvalbumin, myosin, and calmodulin) that may play a role in the regulation of muscle contraction an other enzymatic processes. since most of these proteins also bind Mg2+, it is important to consider the effect that the high free Mg2+ concentration (mM) found in muscle has on the Ca2+ binding properties of these sites. The major effect of Mg2+ is to greatly reduce the rate of Ca2+ binding to the sites that bind Mg2+ and Ca2+ competitively (Ca2+-Mg2+-type sites found in troponin, parvalbumin, and myosin, which would be essentially saturated with Mg2+ in a relaxed muscle) due to the slow dissociation of bound Mg2+. Thus during a transient increase in [Ca2+] similar to that which would occur during muscle activation, these sites would bind very little Ca2+ and, consequently, could not play a regulatory role. Even if Ca2+ were able to bind to these sites during muscle activation (e.g., if the free Mg2+ in muscle is lower than presumed), the dissociation of Ca2+ from these sites would be quite slow due to their very slow off rates for Ca2+, again making these sites unsuitable for participating in a rapid Ca2+-induced switching mechanisms. In contrast, the Ca2+-specific-type (regulatory) sites found in troponin and calmodulin do not have these restraints. The rate of Ca2+ binding to these sites is not affected by Mg2+ and the off rate of Ca2+ from these sites is very rapid due to their lower Ca2+ affinity. Thus, these sites are able to respond to rapid Ca2+ transients, an essential feature for any Ca2+ binding site that plays a regulator role.

Binding Sites↗

PubMed2005

Effects of electrically induced muscle contraction on flexion reflex in human spinal cord injury.

STUDY DESIGN: Flexion reflex study in motor complete human spinal cord injury (SCI). OBJECTIVES: To examine changes in the magnitude of the flexion reflex following functional electrical stimulation (FES) of the rectus femoris (RF) muscle. SETTING: Bioengineering Unit, University of Strathclyde, Glasgow, Scotland, UK. METHODS: The flexion reflex was evoked by electrical stimulation of the sural nerve, and was recorded in the tibialis anterior (TA) muscle. RF muscle conditioning stimulation was performed at 0.7, 1, and 2 times motor threshold ( x MT) over a range of conditioning test intervals. RESULTS: The incidence of the early component of the flexion reflex (<100 ms) was low, suggesting that this reflex component might be suppressed in SCI. The long latency flexion reflex component (>120 ms) was observed in all subjects during control conditions and following sensorimotor conditioning. FES applied to the RF muscle (above and below MT) in the main induced a significant early and long lasting depression of the long latency flexion reflex. CONCLUSION: The depression of the flexion reflex was a result of multisensory actions on flexion reflex pathways resulting from the direct and indirect (mechanical) consequences of electrically induced muscle contraction on cutaneous and muscle afferents. Our findings emphasize the importance of sensory feedback mechanisms in modulating flexion reflex excitability, and highlight the need for rehabilitation professionals to consider the central actions of FES-induced afferent feedback when incorporating FES into a rehabilitation program. SPONSORSHIP: State Scholarships Foundation (IKY) of Hellas.

Adult↗

PubMed1998

Effects of acetylcholine and nitric oxide on forearm blood flow at rest and after a single muscle contraction.

We tested the hypothesis that ACh or nitric oxide (NO) might be involved in the vasodilation that accompanies a single contraction of the forearm. Eight adults (3 women and 5 men) completed single 1-s-duration contractions of the forearm to raise and lower a weight equivalent to approximately 20% maximal voluntary contraction through a distance of 5 cm. In a second protocol, each subject had a cuff, placed completely about the forearm, inflated to 120 mmHg for a 1-s period, then released as a simulation of the mechanical effect of muscle contraction. Three conditions were studied, always in this order: 1) control, with intra-arterial infusion of saline; 2) after muscarinic blockade with atropine; and 3) after NO synthase inhibition with NG-monomethyl-L-arginine (L-NMMA) plus atropine. Forearm blood flow (FBF), measured by combined pulsed and echo Doppler ultrasound, was reduced at rest with L-NMMA-atropine compared with the other two conditions. After the single contraction, there were no effects of atropine, but L-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflation, atropine had no effects, whereas L-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation that L-NMMA reduced FBF in response to both cuff inflation and a brief contraction indicates that NO from the vascular endothelium might modulate the basal level of vascular tone and the mechanical component of the hyperemia with exercise. It is unlikely that ACh and NO from the endothelium are involved in the dilator response to a single muscle contraction.

Acetylcholine↗

PubMed1996

Isometric muscle contractions after double pulse stimulation. comparison of healthy subjects and patients with myotonic dystrophy.

Isometric contractions of the adductor pollicis muscle were studied in healthy subjects and patients with myotonic dystrophy after single and double stimuli of the ulnar nerve using a wide range of interstimulus intervals (ISI, 0.4-180 ms). In healthy subjects, the force contributed by a second stimulus was greater than the single twitch force being maximal (mean + 140%) at 12-ms ISI. In myotonic dystrophy, the force contributed by the second stimulus was (relative to a reduced twitch amplitude) increased (mean + 204%) with a maximum at 4.8-ms ISI. An abnormal increase of force was only recorded if the single twitch force was clearly reduced. The absolute refractory period of muscle contraction (normal range 1.2-1.6 ms, mean 1.35 ms) was shortened in all patients (mean 1.01 ms) except one (1.2 ms). The ISI showing the maximal force were related to those showing the maximal prolongation of the contraction time in healthy subjects (r = 0.71) but not in patients. The rate of force development contributed by a second stimulus was slower than expected from the summation of two single twitches with short stimulus intervals (3-40 ms) a phenomenon called early depression. In patients, the early depression was reduced or abolished within this range of ISI as has been found in dystrophic mouse muscles. The optimal ISI in patients was shifted towards very short times and together with the other disturbances it is suggested that activation of diseased muscle by motoneurons may be less effective, being an additional factor leading to weakness in myotonic dystrophy.

Adult↗

PubMedDate not supplied

[Thin filament elasticity and its role in the muscle contraction].

The available experimental methods do not allow one to establish unambiguously the molecular structural events during muscle contraction. To resolve the existing controversies, I have devised an unconventional original computer program. The new approach allows the reconstruction of the hexagonal lattice of the sarcomere for different muscle states and verification of the structure by comparison of the calculated Fourier spectra with the real diffraction patterns. Previously, by the use of this approach, the real structure of a myosin filament from vertebrate striated muscle has been reconstructed (http://zope.ibib.waw.pl/pspk). In this work, a reconstruction for the thin filament is presented for three states: relaxed, after activation, and during contraction. Good consistency of the calculated Fourier spectra with the real diffraction patterns available in the literature suggests that the thin filament, due to flexibility, plays an active part in muscle contraction, as myosin cross-bridges do.

Actin Cytoskeleton↗

PubMed1998

Regulation of ATP supply during muscle contraction: theoretical studies.

The dynamic computer model of oxidative phosphorylation developed previously and successfully tested for large-scale changes in fluxes and metabolite concentrations was used to study the question of how the rate of ATP production by oxidative phosphorylation is adjusted to meet the energy demand during muscle contraction, which causes a great increase in ATP consumption in relation to the resting state. The changes in the respiration rate and ATP/ADP ratio after the onset of maximal work measured experimentally were compared with simulated changes in the respiration rate and ATP/ADP in several different cases, assuming direct activation of different steps by an external effector. On the basis of the computer simulations performed, it was possible to conclude which enzymes/metabolic blocks should be directly activated to cause the experimentally observable changes in fluxes and metabolite concentrations. The theoretical results obtained suggest that the parallel direct activation of actinomyosin-ATP-ase and oxidative phosphorylation by an external effector (for example calcium ions) is the main mechanism responsible for fitting of ATP production to ATP consumption, while the negative feedback via an increase in ADP concentration (decrease in ATP/ADP), which indirectly activates the ATP supply, plays only a minor role. Additionally, the conclusion is drawn that most of the oxidative phosphorylation steps should be directly activated in order to explain the observed changes in the respiration rate and ATP/ADP ratio (and also in other parameters) during muscle contraction. It is suggested that there should exist a universal external activator/regulatory mechanism which causes a parallel stimulation of different enzymes/processes. A possible nature of such an activator is shortly discussed.

Adenosine Diphosphate↗

PubMed1993

Serotonin-induced muscle contraction in rat stomach fundus is mediated by a G alpha z-like guanine nucleotide binding protein.

Serotonin (5-HT) potently contracts the fundus of the rat stomach; however, the associated transduction pathway has not been described fully. Experiments were performed in an attempt to gain insight into the coupling mechanism associated with this fundal 5-HT receptor. 5-HT-stimulated [35S]GTP gamma S binding to a protein which was recognized by anti-G alpha Z antiserum in a Mg(++)-dependent fashion. 5-HT increased [35S]GTP gamma S binding in the fundus, but not in the corpus of the rat stomach. 5-HT also enhanced the binding of [alpha-32P]GTP to the fundal protein and increased the hydrolysis of GTP to GDP in fundal membranes. The fundal protein which binds GTP is 25 to 29 kDa in size whereas the brain G alpha Z protein which is recognized by the anti-G alpha Z antibody is a 41 kDa protein. Mixing experiments revealed that the fundal guanine nucleotide binding protein does not appear to be a proteolytic product of the 41 kDa G alpha Z protein. Activating protein kinase C with phorbol-12-myristate, 13-acetate induced a concentration-dependent, noncompetitive inhibition of [35S]GTP gamma S binding to the fundal protein, and of 5-HT-induced contraction of fundal strips. Phorbol-12-myristate, 13-acetate did not alter carbachol- or KCl-mediated fundus contraction. Furthermore, the activation of [35S]GTP gamma S binding by serotonergic agonists and its inhibition by pharmacological antagonists corresponded to the known actions of these agents on contraction of fundal muscle. The results provide evidence that the 5-HT receptor in the rat stomach fundus is coupled directly or indirectly to a G alpha z-like protein which may mediate 5-HT-induced contraction in this tissue.

Amino Acid Sequence↗

PubMed1980

Effects of competitive antagonists on phasic and tonic components of vascular smooth muscle contraction.

Phasic and tonic components of contraction are functional properties of vascular smooth muscle reflecting, respectively, release of intracellular calcium and utilization of extracellular calcium. Recently, it has been appreciated that different agonists may manifest discrete actions on these functional properties of vascular smooth muscle. We have analyzed the contractile response of rabbit aortic strips in response to maximal effective concentrations of the agonists norepinephrine, angiotensin II and acetylcholine in the absence and presence of their specific antagonists: phentolamine, saralasin and atropine in order to determine the actions of the antagonists on these functional properties of vascular smooth muscle. When contractions produced by norepinephrine or acetylcholine were plotted as ln velocity vs. time, characteristic curves described by a two-term function Qt = phi 1e-phi 2t + theta 1e-theta 2t were found (Qt = velocity at any time t: phi 1 and theta 1 are velocity of contraction at zero time for phasic and tonic components; phi 2 and theta 2 are contraction velocity constants for their respective components of contraction). The first term represents the phasic component and the second term the tonic component of contraction. The contraction velocity parameters were different for norepinephrine and acetylcholine. Angiotension II-induced contractions gave velocity curves described by a single term, i.e. phasic component of contraction. Phentolamine blocked completely the tonic component and the decreased tension achieved with norepinephrine was completely accounted for by inhibition of the tonic contribution to total tension development. Atropine completely blocked acetylcoholine's tonic component and also attenuated slightly the phasic component. Saralasin reduced angiotensin II-induced tension development and contraction velocity analysis suggested a non-competitive action. We conclude that competitive antagonists may exert distinct actions on the phasic and tonic components of vascular smooth muscle contraction.

Acetylcholine↗

PubMed1994

cAMP-dependent phosphorylation of Aplysia twitchin may mediate modulation of muscle contractions by neuropeptide cotransmitters.

Acting through a cAMP-cAMP-dependent protein kinase (cAPK) cascade, members of two neuropeptide families, the small cardioactive peptides and myomodulins, modulate contraction amplitude and relaxation rate in the accessory radula closer (ARC) muscle of the marine mollusc Aplysia californica. An approximately 750-kDa phosphoprotein was identified in the ARC muscle as the major substrate for cAPK activated either by application of neuropeptides or by peptides released by motorneuron stimulation at physiological frequencies. Immunoblot and immunoelectron microscopy experiments revealed the widespread presence of this protein in Aplysia muscles and its colocalization with contractile filaments in the ARC muscle. Sequence analysis of proteolytic peptide fragments derived from the protein indicated that it is structurally related to the muscle protein twitchin. Finally, the level of neuropeptide-induced phosphorylation of the protein correlated well with peptidergic modulation of the relaxation rate of the muscle. We propose that twitchin in Aplysia, and perhaps in other species, may mediate the modulation of the relaxation rate of muscle contractions.

Amino Acid Sequence↗

PubMed1981

[Influence of muscle contraction on wound measurements after defined dynamic stabbing tests (author's transl)].

The following questions were considered: Are the results of dynamic stabbing tests (experimentally taken from corpses) acceptable for forensic purposes? What about the influence of muscle contraction and wound measurements after defined violence? It could be demonstrated that in dynamic stabbing tests rigor mortis in muscle is equivalent to an extreme muscle contraction. It was easier to perforate a limb with stretched muscles than with relaxed ones. Very seldom people are wounded having stretched their muscles extremely. Therefore, quantitative results of dynamic stabbing tests in corpses represent the minimum of reconstructed stabbing dynamics in vivo.

Forensic Medicine↗

PubMed1996

NMDA receptor blockade in cat dorsal horn blunts reflex pressor response to muscle contraction and stretch.

The role of N-methyl-D-aspartate (NMDA) receptors in the reflex pressor response to static muscle contraction and passive stretch was examined by microdialyzing the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (AP-5) into the L7 or L6 and S1 levels of the dorsal horn of anesthetized cats. Contraction, elicited by electrical stimulation of the cut L7 and S1 ventral roots, increased mean arterial pressure (MAP) and heart rate (HR). Passive stretch at tensions similar to those generated by contraction also increased these variables. These cardiovascular changes were unaffected by dialyzing AP-5 (10 mM) into the dorsal horn at L7. Increasing the syringe concentration of AP-5 to 100 mM attenuated the pressor and HR responses from 62 +/- 8 to 31 +/- 6 mmHg and 18 +/- 4 to 12 +/- 4 beats/min, respectively. AP-5 blunted the increase in MAP (59 +/- 10 vs. 41 +/- 10 mmHg) evoked by muscle stretch. Simultaneously microdialyzing AP-5 (10 or 100 mM) into the dorsal horn at the L6 and S1 spinal levels also blunted the MAP and HR responses to contraction and stretch. These results suggest that NMDA receptors play a role in mediating the MAP and HR responses to static muscle contraction at the spinal level of the central nervous system. Furthermore, these data demonstrate that collaterals from muscle afferents partially mediate the reflex cardiovascular responses evoked by muscle contraction and stretch.

2-Amino-5-phosphonovalerate↗

PubMed1999

The role of the NH(2)- and COOH-terminal domains of the inhibitory region of troponin I in the regulation of skeletal muscle contraction.

The role of the inhibitory region of troponin (Tn) I in the regulation of skeletal muscle contraction was studied with three deletion mutants of its inhibitory region: 1) complete (TnI-(Delta96-116)), 2) the COOH-terminal domain (TnI-(Delta105-115)), and 3) the NH(2)-terminal domain (TnI-(Delta95-106)). Measurements of Ca(2+)-regulated force and relaxation were performed in skinned skeletal muscle fibers whose endogenous TnI (along with TnT and TnC) was displaced with high concentrations of added troponin T. Reconstitution of the Tn-displaced fibers with a TnI.TnC complex restored the Ca(2+) sensitivity of force; however, the levels of relaxation and force development varied. Relaxation of the fibers (pCa 8) was drastically impaired with two of the inhibitory region deletion mutants, TnI-(Delta96-116).TnC and TnI-(Delta105-115).TnC. The TnI-(Delta95-106).TnC mutant retained approximately 55% relaxation when reconstituted in the Tn-displaced fibers. Activation in skinned skeletal muscle fibers was enhanced with all TnI mutants compared with wild-type TnI. Interestingly, all three mutants of TnI increased the Ca(2+) sensitivity of contraction. None of the TnI deletion mutants, when reconstituted into Tn, could inhibit actin-tropomyosin-activated myosin ATPase in the absence of Ca(2+), and two of them (TnI-(Delta96-116) and TnI-(Delta105-115)) gave significant activation in the absence of Ca(2+). These results suggest that the COOH terminus of the inhibitory region of TnI (residues 105-115) is much more critical for the biological activity of TnI than the NH(2)-terminal region, consisting of residues 95-106. Presumably, the COOH-terminal domain of the inhibitory region of TnI is a part of the Ca(2+)-sensitive molecular switch during muscle contraction.

Amino Acid Sequence↗

PubMed1994

Equilibrium linkage analysis of cardiac thin filament assembly. Implications for the regulation of muscle contraction.

A major focus in studies of muscle contraction has been the effect of Ca2+ on the interactions among the thin filament's five constituent polypeptides: actin, tropomyosin, troponin C (TnC), troponin T (TnT), and troponin I (TnI). We have investigated these interactions by analyzing thin filament assembly as a linear lattice binding problem with linkage relationships in the associations of tropomyosin, actin, and troponin. Binding of TnT, the binary TnT.TnI complex, or the ternary troponin complex (+/- Ca2+) to tropomyosin was measured spectrofluorimetrically after labeling cardiac tropomyosin with N-(1-pyrene)iodoacetamide. The affinity constants ranged between 0.2 and 0.6 microM-1 in the presence of 300 mM KCl. Also, the affinities of tropomyosin, tropomyosin-troponin, tropomyosin.TnT, and tropomyosin.TnT.TnI for an isolated site on F-actin were determined. The actin association constants were 0.0006 microM-1 for tropomyosin, 1 microM-1 for tropomyosin.TnT, 2 microM-1 for tropomyosin.TnT.TnI, 0.5 microM-1 for tropomyosin.troponin, and 0.5 microM-1 for tropomyosin-troponin.Ca2+. Linked equilibrium analysis permitted calculation of the affinities for actin.tropomyosin of TnT (400 microM-1), TnT.TnI (1600 microM-1), troponin (500 microM-1), and troponin.Ca2+ (300 microM-1). Therefore, both troponin and tropomyosin.troponin retain high actin-affinity even when Ca2+ is present or when TnI is removed, and even in the absence of cooperative contributions. The results are discussed in consideration of increasing evidence for a Ca(2+)-regulated azimuthal movement of tropomyosin on F-actin (Lehman, W., Craig, R., and Vibert, P. (1994) Nature 368, 65-67). It is proposed that tropomyosin movement may be due to switching between TnI-mediated and TnT-mediated binding of troponin-tropomyosin to distinct sites on F-actin.

Actins↗