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At least 289 records · Page 16Linked to original sources

PubMed2001

Myosin light chain kinase as a multifunctional regulatory protein of smooth muscle contraction.

Myosin light chain kinase (MLCK) is a regulatory protein for smooth muscle contraction, which acts by phosphorylating 20-kDa myosin light chain (MLC20) to activate the myosin ATPase activity. Although this mode of action is well-established, there are numerous reports of smooth muscle contraction that is not associated with MLC20 phosphorylation. The kinase activity for the phosphorylation is localized at the central part of MLCK, which is also furnished with actin-binding activity at its N terminal and myosin-binding activity at its C terminal. This article overviews as to how such multifunctional properties of MLCK modify the actin-myosin interaction and presents our observations that the phosphorylation is not obligatory in induction of smooth muscle contraction.

Actins↗

PubMed1992

The biophysics and biochemistry of smooth muscle contraction.

In this review the biophysics and biochemistry of smooth muscle contraction are dealt with. We describe a new model for the study of bronchial smooth muscle, which facilitates study of cellular contractile mechanisms. A new concept emerging is that study of steady-state mechanical parameters such as maximal isometric force (Po) velocity is inadequate because two types of crossbridges (normally cycling (NBR) and latch) seem to be sequentially active during smooth muscle contraction. Thus quick-release techniques are required to characterize the force-velocity properties of the two types of bridges. Pathophysiological processes that affect the muscle's shortening ability seem to affect the early NBRs only. With respect to maximal shortening capacity of the smooth muscle, the role of loading is very important. The differences between isotonic, elastic, and viscous loading are considerable. Ultimately, the time course and magnitude of loading should exactly resemble that operative in vivo. Once again, it is the characteristic of loading in the early phase of contraction that is crucial, as most of the shortening in smooth muscle occurs early in the contraction. While the maximum force developed by smooth muscle per unit cross-sectional area is the same as for striated muscle, the velocity is 50 times less. The properties of the series and parallel elastic elements of smooth muscle are described. The latter, when in compression mode, acts as an internal resistance to shortening and probably limits it. Isotonic relaxation has therefore not been studied in smooth muscle. We have developed a shortening parameter that is independent of the load on the muscle and of the initial length of the muscle's contractile element. We report the novel observation that isotonically relaxing smooth muscle reactivates itself, resulting in terminal slowing of the relaxation process. With respect to the biochemistry of smooth muscle contraction, contractile (actin isoforms, myosin heavy and light chains and their isoforms), regulatory (calmodulin-4 Ca2+, myosin light chain kinase, myosin light chain and its phosphorylation, tropomyosin, caldesmon, and calponin), and cytoskeletal (chiefly desmin and vimentin) proteins are discussed. While the kinase activates the contractile system, caldesmon and calponin modulate the activity downward. The cytoskeletal proteins desmin, vimentin, and alpha-actinin could constitute the muscle cell's internal resistor.

Animals↗

PubMed2002

The role of troponins in muscle contraction.

Troponin (Tn) is the sarcomeric Ca2+ regulator for striated (skeletal and cardiac) muscle contraction. On binding Ca2+ Tn transmits information via structural changes throughout the actin-tropomyosin filaments, activating myosin ATPase activity and muscle contraction. Although the Tn-mediated regulation of striated muscle contraction is now well understood, the role of different Tn isoforms in these processes is the subject of intensive investigations. This review addresses the physiological significance of the multiple Tn isoforms in skeletal and cardiac muscles as well as their role in the regulation of contraction.

Amino Acid Sequence↗

PubMed1970

Conversion of glycogen phosphorylase b to a by non-activated phosphorylase b kinase: an in vitro model of the mechanism of increase in phosphorylase a activity with muscle contraction.

Phosphorylase b kinase activity, as present in resting muscle in the non-activated form, appears to be ample to account for the fast appearance of phosphorylase a observed with muscle contraction. The kinase activity is repressed by free ATP and stimulated by free Mg(2+). Phosphorylase b kinase activity increases greatly when the Mg(2+):ATP ration exceeds 1. It is proposed that the breakdown of ATP that occurs during muscle contraction may represent the triggering factor for the observed in vivo conversion of phosphorylase b into a.

Adenosine Triphosphate↗

PubMed1984

Intracellular mechanism of quinidine action on muscle contraction. A comparison between rabbit cardiac and skeletal muscle.

The mechanism of quinidine action on rabbit cardiac and skeletal muscle was examined with "functionally skinned" muscle-fiber preparations. By using these preparations we could correlate measurements of muscle tension with the effect of quinidine on the Ca2+ activation of the contractile proteins and on the Ca2+ uptake and release from the sarcoplasmic reticulum (SR).

Animals↗

PubMed2006

Mechanomyographic and electromyographic responses to eccentric muscle contractions.

Little is known regarding the modulation of torque during eccentric muscle actions. Mechanomyographic (MMG) and electromyographic (EMG) signals have been used to examine motor control strategies. The purpose of this study was to examine the MMG and EMG amplitude and frequency in relation to torque during eccentric muscle contractions. Eight women performed eccentric leg extension muscle contractions at 10-100% of peak torque (PT). A piezoelectric crystal contact sensor and bipolar surface electrodes were placed on the vastus medialis to detect the MMG and EMG signals. Polynomial regression analyses indicated that EMG amplitude (r(2)=0.994) and MMG wavelet center frequency (CF) (r(2)=0.846) increased linearly to 100% eccentric PT, whereas there were no significant relationships for EMG wavelet CF or MMG amplitude and eccentric torque. These results suggested that eccentric torque is primarily modulated through changes in motor unit firing rate.

Adult↗

PubMed1998

Ventrolateral medullary control of cardiovascular activity during muscle contraction.

An overview of the role of ventrolateral medulla (VLM) in regulation of cardiovascular activity is presented. A summary of VLM anatomy and its functional relation to other areas in the central nervous system is described. Over the past few years, various studies have investigated the VLM and its involvement in cardiovascular regulation during static muscle contraction, a type of static exercise as seen, for example, during knee extension or hand-grip exercise. Understanding the neural mechanisms that are responsible for regulation of cardiovascular activity during static muscle contraction is of particular interest since it helps understand circulatory adjustments in response to an increase in physical activity. This review surveys the role of several receptors and neurotransmitters in the VLM that are associated with changes in mean arterial pressure and heart rate during static muscle contraction in anesthetized animals. Possible mechanisms in the VLM that modulate cardiovascular changes during static muscle contraction are summarized and discussed. Localized administration of an excitatory amino-acid antagonist into the rostral portion of the VLM (RVLM) attenuates increases in blood pressure and heart rate during static muscle contraction, whereas its administration into the caudal part of the VLM (CVLM) augments these responses. Opioid or 5-HT1A receptor stimulation in the RVLM, but not in the CVLM, attenuates cardiovascular responses to muscle contraction. Furthermore, intravenous, intracerebroventricular or intracisternal injection of an alpha 2-adrenoceptor agonist or a cholinesterase inhibitor attenuates increases in blood pressure and heart rate during static muscle contraction. Finally, the possible involvement of endogenous neurotransmitters in the RVLM and the CVLM associated with cardiovascular responses during static muscle contraction is discussed. An overview of the role of the VLM in the overall cardiovascular control network in the brain is presented and critically reviewed.

Animals↗

PubMed2005

Do dorsal head contact forces have the potential to identify impairment during graded craniocervical flexor muscle contractions?

OBJECTIVE: To determine if the force exerted onto the supporting surface by the dorsal head during graded contractions of isometric craniocervical flexion (ICCF) in the supine position has the potential to measure aberrant muscle performance between participant groups with and without painful neck disorders. DESIGN: Cross-sectional, between-participant study of the force exerted by the head on the supporting surface during ICCF muscle contractions. SETTING: Research laboratory. PARTICIPANTS: Thirty-two participants with a history of neck pain and 32 asymptomatic control participants. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: Dorsal head force (DHF), which is the force (in newtons) exerted by the head on the supporting surface during ICCF muscle contractions in the supine position. ICCF muscle contractions were performed at maximal voluntary contraction (MVC), and sustained at contractions of 50% of MVC and 20% of MVC. RESULTS: Both neck pain and control participants significantly increased their DHF on the supporting surface from resting values during all ICCF muscle contractions (P<.001). No differences in DHF were found between symptomatic and control participants during any of the ICCF efforts. CONCLUSIONS: It would appear that DHF exerted on the supporting surface during graded ICCF muscle contractions is similar between neck pain sufferers and control participants, and is therefore limited in its usefulness as a measurement of abnormal performance.

Adult↗

PubMed2004

8-Bromo-cAMP decreases the Ca2+ sensitivity of airway smooth muscle contraction through a mechanism distinct from inhibition of Rho-kinase.

To clarify whether cyclic AMP (cAMP)/cAMP-dependent protein kinase (PKA) activation and Rho-kinase inhibition share a common mechanism to decrease the Ca2+ sensitivity of airway smooth muscle contraction, we examined the effects of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP), a stable cAMP analog, and (+)-(R)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexane carboxamide dihydrochloride, monohydrate (Y-27632), a Rho-kinase inhibitor, on carbachol (CCh)-, guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS)-, 4beta-phorbol 12,13-dibutyrate (PDBu)-, and leukotriene D4 (LTD4)-induced Ca2+ sensitization in alpha-toxin-permeabilized rabbit tracheal and human bronchial smooth muscle. In rabbit trachea, CCh-induced smooth muscle contraction was inhibited by 8-BrcAMP and Y-27632 to a similar extent. However, GTPgammaS-induced smooth muscle contraction was resistant to 8-BrcAMP. In the presence of a saturating concentration of Y-27632, PDBu-induced smooth muscle contraction was completely reversed by 8-BrcAMP. Conversely, PDBu-induced smooth muscle contraction was resistant to Y-27632. In the presence of a saturating concentration of 8-BrcAMP, GTPgammaS-induced Ca2+ sensitization was also reversed by Y-27632. The 8-BrcAMP had no effect on the ATP-triggered contraction of tracheal smooth muscle that had been treated with calyculin A in rigor solutions. The 8-BrcAMP and Y-27632 additively accelerated the relaxation rate of PDBu- and GTPgammaS-treated smooth muscle under myosin light chain kinase-inhibited conditions. In human bronchus, LTD4-induced smooth muscle contraction was inhibited by both 8-BrcAMP and Y-27632. We conclude that cAMP/PKA-induced Ca2+ desensitization contains at least two mechanisms: 1) inhibition of the muscarinic receptor signaling upstream from Rho activation and 2) cAMP/PKA's preferential reversal of PKC-mediated Ca2+ sensitization in airway smooth muscle.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1982

Biphasic amphetamine effects on skeletal muscle contractions: noncholinergic mechanisms.

Noncholinergic mechanisms underlying the biphasic effects of (+)-amphetamine on skeletal muscle contractions were studied in the directly-stimulated, cholinergically blocked, rat phrenic nerve-diaphragm preparation. Low (2.7-8.1 x 10(-4)M) and high (10.8-21.6 x 10(-4)M) levels of (+)-amphetamine produced concentration-dependent enhancement and blockade of muscle contractions, respectively, in tissues pretreated with alpha-bungarotoxin, beta-bungarotoxin, or (+)-tubocurarine. These biphasic effects were not modified by tyramine, phentolamine, or propranolol arguing against a mechanism involving a direct or indirect adrenoceptor interaction. Amphetamine did not modify (Na+-K+)-stimulated ATPase activity. Increased [K+] or decreased [Na+] antagonized (+)-amphetamine enhancement of contractions and potentiated blockade; similar effects were observed after high concentration amantadine or procaine pretreatment. K+-free media potentiated (+)-amphetamine facilitation of contractions as did low concentrations of amantadine or procaine. These results suggest that amphetamine may biphasically modify skeletal muscle contractions by interactions involving the movements of Na+ and K+ independent of (Na+-K+)-stimulated ATPase.

Amantadine↗

PubMed1994

Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits.

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

Animals↗

PubMed1970

Effect of speed of muscle contraction on physiological tremor in normal subjects and in patients with thyrotoxicosis and myxoedema.

The speed of the ankle jerk and physiological finger tremor in patients with thyrotoxicosis and myxoedema have been compared with those in age-matched control subjects. Tremor amplitude depends on the speed of muscle contraction; the faster muscle contracts the greater is the amplitude of tremor, and vice versa. The frequency of the dominant tremor peak is not affected by the speed of contraction but its size increases as muscle contracts faster. Muscle dynamics is clearly one of many factors influencing physiological tremor but is not responsible for the dominant frequency of tremor at round 9 c/sec.

Ankle↗

PubMed2000

Remote arteriolar dilations in response to muscle contraction under capillaries.

In hamster cremaster muscle, it has been shown previously that contraction of skeletal muscle fibers underlying small groups of capillaries (modules) induces dilations that are proportional to metabolic rate in the two arteriolar generations upstream of the stimulated capillaries (Berg BR, Cohen KD, and Sarelius IH. Am J Physiol Heart Circ Physiol 272: H2693-H2700, 1997). These remote dilations were hypothesized to be transmitted via gap junctions and not perivascular nerves. In the present study, halothane (0.07%) blocked dilation in the module inflow arteriole, and dilation in the second arteriolar generation upstream, the branch arteriole, was blocked by both 600 mosM sucrose and halothane but not tetrodotoxin (2 microM). Dilations in both arterioles were not blocked by the gap junction uncoupler 18-beta-glycyrrhetinic acid (40 microM), and 80 mM KCl did not block dilation of the module inflow arteriole. These data implicate a gap junctional-mediated pathway insensitive to 18-beta-glycyrrhetinic acid in dilating the two arterioles upstream of the capillary module during "remote" muscle contraction. Dilation in the branch arteriole, but not the module inflow arteriole, was attenuated by 100 microM N(omega)-nitro-L-arginine. Thus selective contraction of muscle fibers underneath capillaries results in dilations in the upstream arterioles that have characteristics consistent with a signal that is transmitted along the vessel wall through gap junctions, i.e., a conducted vasodilation. The observed insensitivities to 18-beta-glycyrrhetinic acid, to KCl, and to N(omega)-nitro-L-arginine suggest, however, that there are multiple signaling pathways by which remote dilations can be initiated in these microvessels.

Animals↗

PubMed1992

Pharyngeal dilation associated with cricothyroid muscle contraction in dogs.

The mechanical function of phasic respiratory-related activity of the cricothyroid muscle of the larynx is poorly understood. We studied five adult cross-bred dogs (weight 14-20 kg) deeply anesthetized with pentobarbitone sodium, mechanically ventilated via a tracheostomy, and placed prone with the mouth open. Bilateral cricothyroid muscle contraction was induced by supramaximal electrical stimulation of the external branches of the superior laryngeal nerve. Computerized axial tomography was used to assess effects of cricothyroid muscle contraction. During cricothyroid muscle contraction, oropharyngeal (tip of epiglottis) cross-sectional area increased by 18.0 +/- 3.0% (SE) (P = 0.008), whereas combined left and right piriform recess cross-sectional area increased by 85 +/- 25% (n = 4; P = 0.02) at the midepiglottic level and by 152 +/- 37% (P = 0.01) at the base of the epiglottis. Furthermore, at the base of the epiglottis the maximum horizontal distance between the alae of the thyroid cartilage increased by 21 +/- 8% (P = 0.05). In contrast, lateral glottic diameter decreased by 52 +/- 2% (n = 4; P = 0.01), whereas dorsoventral glottic diameter increased by 18 +/- 5% (n = 4; P less than 0.02). The cricothyroid muscle, therefore, has the capacity to act simultaneously as a pharyngeal dilator and a glottic constrictor and thus may play a role in the control of oropharyngeal as well as laryngeal patency.

Animals↗

PubMed2003

Inhibition of smooth muscle contraction by magnolol and honokiol in porcine trachea.

Magnolol and honokiol are the two major phenolic constituents of the plant medicine "Houpo" ( Magnolia obovata), which is used in the treatment of chest tightness and asthma. The aim of this study was to investigate the influence of magnolol and honokiol on smooth muscle tone in porcine trachea. Magnolol and honokiol (0.1 - 100 microM) inhibited carbachol- and high K +-induced muscle contractions in a concentration-dependent fashion, but did not affect basal muscle tension. After washout of these pretreatments, carbachol- and high K +-evoked muscle contractions were still abolished, suggesting that the inhibition was irreversible. Magnolol and honokiol also concentration-dependently decreased the Ca 2+-dependent muscle contraction induced by high K + depolarization. Ca 2+ channel antagonists attenuated carbachol-induced muscular response by approximately 30 %, but did not further potentiate the inhibitory actions of magnolol and honokiol on muscle contraction. However, the inhibitory effects of magnolol and honokiol on carbachol-evoked muscular contractile response were partially reversed after removal of Ca 2+ channel antagonist pretreatment. Alternatively, caffeine-elicited muscle contractions were not altered by magnolol, honokiol, and verapamil. In conclusion, the relaxant effects of magnolol and honokiol on porcine tracheal smooth muscle suggest an association with the blockade of Ca 2+ influx through voltage-operated Ca 2+ channels instead of Ca 2+ release from intracellular Ca 2+ stores. The magnolol- and honokiol-induced inhibitions on tracheal smooth muscle contraction may be relevant to the claimed therapeutic effects of the extract from magnolia bark and contribute to their pharmacological effects by acting as anti-asthmatic agents.

Animals↗

PubMed2006

Neuregulins mediate calcium-induced glucose transport during muscle contraction.

Neuregulin, a growth factor involved in myogenesis, has rapid effects on muscle metabolism. In a manner analogous to insulin and exercise, neuregulins stimulate glucose transport through recruitment of glucose transporters to surface membranes in skeletal muscle. Like muscle contraction, neuregulins have additive effects with insulin on glucose uptake. Therefore, we examined whether neuregulins are involved in the mechanism by which muscle contraction regulates glucose transport. We show that caffeine-induced increases in cytosolic Ca2+ mediate a metalloproteinase-dependent release of neuregulins, which stimulates tyrosine phosphorylation of ErbB4 receptors. Activation of ErbB4 is necessary for Ca2+-derived effects on glucose transport. Furthermore, blockage of ErbB4 abruptly impairs contraction-induced glucose uptake in slow twitch muscle fibers, and to a lesser extent, in fast twitch muscle fibers. In conclusion, we provide evidence that contraction-induced activation of neuregulin receptors is necessary for the stimulation of glucose transport and a key element of energetic metabolism during muscle contraction.

Animals↗

PubMed2004

Role of Ca2+ in vascular smooth muscle contractions induced by Phoneutria nigriventer spider venom.

Phoneutria nigriventer venom (PNV) contracts vascular tissues and increases arterial blood pressure. This study aimed to investigate the mechanisms involved on PNV-induced contractions of rabbit mesenteric and celiac arteries. Strips of mesenteric and celiac arteries were suspended in a cascade system and superfused with warmed and oxygenated Krebs solution. PNV was dialyzed in order to exclude the participation of biogenic amines in the contractions elicited by the venom. Noradrenaline (NA, 30-300 pmol), PNV (1-10 microg), Bay K-8644 (0.3-3 nmol) and KCl (10-100 micromol) dose-dependently contracted the preparations. Ca(2+)-free solution reduced by 38 and 83% the PNV-induced contractions of mesenteric and celiac arteries, respectively. Subsequent infusion of EGTA (0.2 mM) suppressed the residual contractions. Nifedipine (1 microM) and verapamil (10 microM) abolished PNV- and Bay K-8644-evoked contractions, whereas those induced by NA were reduced to a lesser extent. Lanthanum chloride (0.2 mM) inhibited by 75-90% the mesenteric and celiac contractions mediated by PNV. Caffeine (2 mM) fully blocked contractions induced by NA (95% mean inhibition), but only partly reduced those induced by PNV (35% mean inhibition). Ryanodine (10 microM) inhibited by 50% the contractions evoked by NA, but had no effect on the PNV-induced contractions in both tissues. Our findings indicate that PNV contracts vascular smooth muscle mainly due to increased influx of Ca(2+) from extracellular sources.

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

PubMed1998

[Study of molecular mechanisms of muscle contraction using polarization fluorometry].

The review summarizes results of studies on the conformational changes in contractile proteins during muscle contraction. The studies were carried out by polarized fluorescence technique in the UV and visible light. The revealed were alterations of actin and myosin in muscle fiber, taking place at various stages of contractile cycle. Transition from a weak binding state of actomyosin to a strong one was accompanied by F-actin subunit rearrangements, with C- and N-terminals moving relative to the core of thin filament. Myosin light chains and 20-kDa domain of myosin head moved in the same direction as C- and N-terminal regions of actin. The flexibility of actin filaments increased, whereas that of C- and N-terminal regions decreased sharply. Actin-myosin interaction changed dramatically tropomyosin flexibility and caused displacement of the protein relative to C- and N-terminals of actin. Actin structure "freezing" by glutaraldehyde or phalloidin, actin cleavage by subtilisin, as well as actin alteration in denervational atrophy inhibited markedly the intramolecular movement and isometric tension of muscle contraction. Besides, troponin-, caldesmon-, calponin-, and myosin-systems, regulating muscle contraction, modified actomyosin rearrangements in a Ca(2+)-dependent manner. The role of the movement of polypeptide chains in contractile proteins during muscle contraction is discussed.

Actins↗