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PubMedDate not supplied

[Molecular mechanism of muscle contraction: the straightening of the bent actomyosin bond].

A new molecular mechanism of muscle contraction is considered based on the cyclochelate oxyphosphorane structure of the long-lived intermediate in myosin-catalyzed ATP. Mg hydrolysis proposed earlier by the author. The mechanism implies the steric cleavage of the actomyosin bond by the gamma-phosphoryl group of ATP.Mg tightly binding to myosin; the myosin-catalyzed addition of water to the gamma-phosphoryl group to give oxyphosphorane group which sterically allows the formation of a more weak bent (deformed) actomyosin bond; the actin-catalyzed breakdown of the tightly bound oxyphosphorane intermediate into weakly bound products; the straightening of the bent actomyosin bond with the active change of an angle of myosin head attachment, the liberation of the weakly bound products and the displacement of the actin filament. The data are given in favour of an oxyphosphorane structure of the long-lived intermediate.

Actomyosin↗
PubMed1998

Studies on the effects of piperidine derivatives on blood pressure and smooth muscles contractions.

Ten substituted phenacyl derivatives of 4-hydroxypiperidine were synthesized and studied for their effects on the mean arterial blood pressure (MABP) in normotensive anaesthetized rats and smooth muscles contractions of isolated rabbit jejunum. Two derivatives caused fall in blood pressure at the dose of 10-20 mg/kg and one rise in blood pressure at the dose of 20 mg/kg. Two compounds exhibited biphasic response (hypotensive followed by hypertensive) and one gave triphasic response at 10 mg/kg dose. Rest of four derivatives were found devoid of any effect on mean arterial blood pressure up to the dose of 30 mg/kg. All the derivatives except two caused relaxant effect on the spontaneous contraction of rabbit jejunum at the dose range of 0.1-2 mg/kg.

Animals↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed2003

sup-9, sup-10, and unc-93 may encode components of a two-pore K+ channel that coordinates muscle contraction in Caenorhabditis elegans.

Genetic studies of sup-9, unc-93, and sup-10 strongly suggest that these genes encode components of a multi-subunit protein complex that coordinates muscle contraction in Caenorhabditis elegans. We cloned sup-9 and sup-10 and found that they encode a two-pore K+ channel and a novel transmembrane protein, respectively. We also found that UNC-93 and SUP-10 colocalize with SUP-9 within muscle cells, and that UNC-93 is a member of a novel multigene family that is conserved among C. elegans, Drosophila, and humans. Our results indicate that SUP-9 and perhaps other two-pore K+ channels function as multiprotein complexes, and that UNC-93 and SUP-10 likely define new classes of ion channel regulatory proteins.

Amino Acid Sequence↗
PubMed1983

Changes in the X-ray reflections from contracting muscle during rapid mechanical transients and their structural implications.

During normal contractions of vertebrate striated muscle, it is believed that the cross-bridges which produce the sliding force undergo asynchronous cyclical changes in their structure. Thus, an X-ray diffraction diagram from a muscle under these conditions will give structural information averaged over the whole range of cross-bridge states. Such diagrams show characteristic and informative differences from those given by relaxed muscle, but can give little information about changes in the configuration of the cross-bridges at different stages of their working stroke. However, it is possible to effect a partial synchronization of these changes by applying very rapid changes in length, completed in less than one millisecond to an otherwise isometrically contracting muscle. If the amplitude of these length changes is comparable to the length of the cross-bridge stroke (say 100 A per half-sarcomere), then it should bring about a transient but significant redistribution of cross-bridge states, which would show up in the X-ray diagram. We have made use of synchrotron radiation as a high intensity X-ray source in order to record such patterns with the necessary time resolution (1 ms or less) and have found major changes in the intensity of the 143 A meridional reflection accompanying the rapid length changes of the muscle. These changes appear to arise from specific configurational changes in the cross-bridges during the working stroke. A model is suggested in which the 143 A meridional intensity in a contracting muscle arises mainly from attached cross-bridges and is generated by the part of the myosin head near the S1-S2 junction. During normal contraction, cross-bridges go through their structural cycle asynchronously with each other, since they start at different times, but if the S2 changes in length rather little, then the configurational changes in the myosin heads are synchronized with the actin filament movement in such a way that the S1-S2 junction remains relatively fixed in its axial position. In a quick release, it is suggested that bringing many S1 heads simultaneously to the end of their working strokes on actin disrupts the 143 A axial repeat of their distal ends near S2, and brings about the large decrease of the 143 A meridional reflection. This model therefore involves a large change in the position of part of the myosin head structure relative to actin during the working stroke of the cross-bridge.

Animals↗
PubMed1995

Modulation of the buccal muscle contraction by identified serotonergic and peptidergic neurons in the snail Achatina fulica

Serotonergic and peptidergic modulation of buccal muscle contraction at an identified neuromuscular synapse in the African giant snail Achatina fulica was examined. A pair of excitatory motoneurons of the radula protractor was identified in the buccal ganglia and these were named B10 neurons. Pharmacological experiments revealed the B10s to be cholinergic. The serotonergic cerebral neuron v-CDN enhanced B10-evoked contraction of the radula protractor, and it is suggested that this effect is mediated postsynaptically by serotonin released from the v-CDN terminals. Immunohistochemical analyses revealed that the B10 motoneurons contained an Achatina cardioexcitatory peptide-1 (ACEP-1)-like substance in their cell body, axon and terminals in the radula protractor. From electron microscopic observation, the ACEP-1-like immunoreactive substance was found to be localized in dense-cored vesicles but not in clear vesicles in the nerve terminals. ACEP-1 applied to the radula protractor markedly enhanced B10-evoked contraction of the muscle by increasing the amplitude of excitatory junction potentials (EJPs). The increase of EJP amplitude in the presence of the peptide was probably due to the increased release of acetylcholine from the terminals of B10. It is suggested that the cholinergic motoneuron B10 uses ACEP-1 as an excitatory cotransmitter.

Journal Article↗
PubMed2002

Inhibition of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo.

AIM: To investigate the effect of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo. METHODS: (1) Rabbit tracheas were incubated in organ baths filled with Krebs solution and supplied with a mixed gas of 95 % O2 and 5 % CO2. The isometric force was measured by ink-writing recorders. (2) The incubation period of asthma induced by histamine and acetylcholine (ACh) in guinea pig were measured before and after beta-estradiol (1 mg/kg) were given intramuscularly. RESULTS: (1) Administration of beta-estradiol (0.1 mmol/L) caused relaxation of isolated trachea muscle strips (TMS) in rabbits pre-contracted by ACh and KCl (39 % +/- 5 % and 45 % +/- 19 %). The presence of indomethacin or methylene blue partly decreased the relaxation to beta-estradiol (26 % +/- 8 % and 28 % +/- 13 %), but Nomega-nitro-L-arginine (L-NNA) and propranolol and epithelium removal did not affect it (38 % +/- 10 %, 40 % +/- 15 %, 37 % +/- 8 %). beta-Estradiol can shifted the concentration-response curves of ACh and CaCl2 to the rightward (pD2 = 3.98 and 4.75). In addition, it could also significantly inhibit the contraction of phase caused by ACh, but did not affect the contraction of phase II caused by CaCl2. (2) The incubation period of asthma in guinea pig were delayed by beta-estradiol (1 mg/kg) given intramuscularly. CONCLUSION: (1) The relaxation of beta-estradiol in vitro was epithelium independent and associated with the inhibition of potential-dependent channel and release of Ca2+ from sarcoplasm reticulum induced by ACh. In addition, release of prostaglandins from trachea smooth muscle cells and relaxation through cGMP approach were also included. beta-Adrenoceptor-mediated relaxation was not involved. (2) beta-Estradiol can relax the trachea in vivo in guniea pig.

Acetylcholine↗
PubMed1998

Role of intracellular Ca2+ stores in the inhibitory effect of halothane on airway smooth muscle contraction.

BACKGROUND: Halothane directly inhibits contraction of airway smooth muscle, mainly by decreasing the intracellular concentration of free Ca2+ ([Ca2+]i). The role of intracellular Ca2+ stores, sarcoplasmic reticulum, is still unclear. We investigated the role of sarcoplasmic reticulum in the inhibitory effect of halothane on contraction of airway smooth muscle by measuring [Ca2+]i and intracellular concentration of inositol 1,4,5-triphosphate ([IP3]i), a second messenger for release of Ca2+ from sarcoplasmic reticulum. METHODS: [Ca2+]i was monitored by measuring the 500-nm light emission ratio (F340/F380) of a Ca2+ indicator fura-2 with isometric tension of canine tracheal smooth muscle strip. During Ca2+-free conditions, carbachol (10(-5) M) was introduced with pretreatment of halothane (0-3%). During Ca2+-free conditions, 20 mM caffeine, a Ca2+-induced Ca2+ release channel opener, was introduced with or without halothane. We measured [IP3]i during exposure to carbachol and halothane by radioimmunoassay technique. RESULTS: Pretreatment with halothane significantly diminished carbachol-induced increases in [Ca2+]i by 77% and muscle tension by 83% in a dose-dependent manner. Simultaneous administration of halothane significantly enhanced caffeine-induced transient increases in [Ca2+]i and muscle tension in a dose-dependent manner, by 97% and 69%, respectively. Pretreatment with halothane abolished these responses. Rapid increase in [IP3]i produced by carbachol was significantly inhibited by 32% by halothane in a dose-dependent manner. CONCLUSIONS: Halothane, during Ca2+-free conditions, inhibits transient contraction of airway smooth muscle induced by muscarinic receptor stimulation, mainly by attenuating the increase in [Ca2+]i. Depletion of Ca2+ from sarcoplasmic reticulum via Ca2+-induced Ca2+ release channels also may contribute to the attenuation of the increase in [Ca2+]i by halothane.

Anesthetics, Inhalation↗
PubMed1997

Critical review of the swinging crossbridge theory and of the cardinal active role of water in muscle contraction.

A critical analysis is presented of the experimental findings that led to the sliding filament model and to its offspring--the swinging (by rotating or tilting) crossbridge theory of muscle contraction (SCBT). Several principles that have been taken for granted implicitly and explicitly by the creators of these dogmas are discussed. The failure of numerous efforts to verify predictions of the SCBT, particularly the idea that the myosin molecules undergo a major conformational change, is critically reviewed. Analysis of various experimental data suggests that water may play an active role in muscular contraction. Examination of both the experiments that do not fulfill the expectations of the SCBT and the measurements of water liberation during the "contractile" process suggests a new outlook according to which tension development and movement are not due to major conformational changes but rather to restructuring of the hydration shells of actin and myosin.

Actin Cytoskeleton↗