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PubMed1998

Immediate response of retinal vessels to isometric muscle contraction.

Isometric muscle contraction results in a rise in systemic blood pressure (BP) and constriction of retinal arterioles. The responses in the anaesthetised cat have been studied to provide further insight into the results of human studies. Constriction (median 3.43% of control values) and dilatation (median 4.17% of control values) were observed; the onset of constriction was delayed by 4 s compared with dilatation. There was spatial and temporal variation in the observed calibre changes, and inter-experimental variation in the calibre change/BP ratio. It is concluded that the response of retinal arterioles of measurable size is not unified, and that the two modes of response differ in mechanism.

Animals↗
PubMed1996

Control of energy metabolism during muscle contraction.

Skeletal muscle energetics can be studied noninvasively at rest, during exercise, and in recovery using phosphorus nuclear magnetic resonance (31P-NMR). In resting muscle, inorganic phosphate (P(i)) and total cellular phosphate concentration are regulated by Na(+)-dependent P(i) transport. Insulin was shown to stimulate P(i) uptake in G-8 muscle cells, in isolated rat soleus muscle, and in human muscle in vivo under conditions of hyperinsulinemic-euglycemic clamp. The relationship between plasma P(i) and intracellular muscle P(i) was examined in a group of patients with elevated plasma P(i) resulting from renal failure. The total creatine content of muscle cells is controlled by an active creatine uptake in which beta 2-receptor stimulation and the activity of the Na(+)-K(+)-ATPase play a significant role. Recovery after exercise is entirely oxidative; the rate of ATP synthesis is largely controlled by ADP, the concentration of which is determined by the creatine kinase equilibrium that includes the concentration of H+. At the onset of aerobic dynamic exercise, ATP is maintained largely by glycolysis, producing lactic acid, and by phosphocreatine breakdown. After vasodilation, ATP synthesis becomes predominantly oxidative. The above processes can be quantitatively evaluated by 31P-NMR.

Animals↗
PubMed2002

Signal transduction and protein phosphorylation in smooth muscle contraction.

Smooth muscles are important constituents of vertebrate organisms that provide for contractile activity of internal organs and blood vessels. Basic molecular mechanism of both smooth and striated muscle contractility is the force-producing ATP-dependent interaction of the major contractile proteins, actin and myosin II molecular motor, activated upon elevation of the free intracellular Ca2+ concentration ([Ca2+](i)). However, whereas striated muscles display a proportionality of generated force to the [Ca2+](i) level, smooth muscles feature molecular mechanisms that modulate sensitivity of contractile machinery to [Ca2+](i). Phosphorylation of proteins that regulate functional activity of actomyosin plays an essential role in these modulatory mechanisms. This provides an ability for smooth muscle to contract and maintain tension within a broad range of [Ca2+](i) and with a low energy cost, unavailable to a striated muscle. Detailed exploration of these mechanisms is required to understand the molecular organization and functioning of vertebrate contractile systems and for development of novel advances for treating cardiovascular and many other disorders. This review summarizes the currently known and hypothetical mechanisms involved in regulation of smooth muscle Ca2+-sensitivity with a special reference to phosphorylation of regulatory proteins of the contractile machinery as a means to modulate their activity.

Actins↗
PubMed2006

X-ray interference studies of crossbridge action in muscle contraction: evidence from muscles during steady shortening.

During normal muscle shortening, the myosin heads must undergo many cycles of interaction with the actin filaments sliding past them. It is important to determine what range of configurations is found under these circumstances, and, in terms of the tilting lever arm model, what range of orientations the lever arms undergo. We have studied this using the X-ray interference technique described in the previous article, focusing mainly on the changes in the first order meridional reflection (M3) as compared to isometric. The change in ratio of the heights of the interference peaks indicates how far the mean lever arm angle has moved towards the end of the working stroke; the total intensity change depends on the angle change, on the number of heads now attached at any one time, and on the dispersion of lever arm angles. The latter provides a measure of the distance over which myosin heads remain attached to actin as they go through their working strokes. Surprisingly, the mean position of the attached heads moves only about 1 nm inwards (towards the center of the A-band) at low velocity shortening (around 0.9 T0): their dispersion changes very little. This shows that they must be detaching very early in the working stroke. However, at loads around 0.5 T0, the mean lever arm angle is about half way towards the end of the working stroke, and the dispersion of lever arm angles (with a uniform dispersion) is such as to distribute the heads throughout the whole of the working stroke. At higher velocities of shortening (at 0.3 T0), the mean position shifts further towards the end of the stroke, and the dispersion increases further. The details of the measurements, together with other data on muscle indicate that the force-generating mechanism within the myosin heads must have some unexpected properties.

Animals↗
PubMed2006

Dual roles of tropomyosin as an F-actin stabilizer and a regulator of muscle contraction in Caenorhabditis elegans body wall muscle.

Tropomyosin is a well-characterized regulator of muscle contraction. It also stabilizes actin filaments in a variety of muscle and non-muscle cells. Although these two functions of tropomyosin could have different impacts on actin cytoskeletal organization, their functional relationship has not been studied in the same experimental system. Here, we investigated how tropomyosin stabilizes actin filaments and how this function is influenced by muscle contraction in Caenorhabditis elegans body wall muscle. We confirmed the antagonistic role of tropomyosin against UNC-60B, a muscle-specific ADF/cofilin isoform, in actin filament organization using multiple UNC-60B mutant alleles. Tropomyosin was also antagonistic to UNC-78 (AIP1) in vivo and protected actin filaments from disassembly by UNC-60B and UNC-78 in vitro, suggesting that tropomyosin protects actin filaments from the ADF/cofilin-AIP1 actin disassembly system in muscle cells. A mutation in the myosin heavy chain caused greater reduction in contractility than tropomyosin depletion. However, the myosin mutation showed much weaker suppression of the phenotypes of ADF/cofilin or AIP1 mutants than tropomyosin depletion. These results suggest that muscle contraction has only minor influence on the tropomyosin's protective role against ADF/cofilin and AIP1, and that the two functions of tropomyosin in actin stability and muscle contraction are independent of each other.

Actins↗
PubMed2005

Actin cytoskeletal dynamics in smooth muscle contraction.

Smooth muscles develop isometric force over a very wide range of cell lengths. The molecular mechanisms of this phenomenon are undefined, but are described as reflecting "mechanical plasticity" of smooth muscle cells. Plasticity is defined here as a persistent change in cell structure or function in response to a change in the environment. Important environmental stimuli that trigger muscle plasticity include chemical (e.g., neurotransmitters, autacoids, and cytokines) and external mechanical signals (e.g., applied stress and strain). Both kinds of signals are probably transduced by ionic and protein kinase signaling cascades to alter gene expression patterns and changes in the cytoskeleton and contractile system. Defining the signaling mechanisms and effector proteins mediating phenotypic and mechanical plasticity of smooth muscles is a major goal in muscle cell biology. Some of the signaling cascades likely to be important include calcium-dependent protein kinases, small GTPases (Rho, Rac, cdc42), Rho kinase, protein kinase C (PKC), Src family tyrosine kinases, mitogen-activated protein (MAP) kinases, and p21 activated protein kinases (PAK). There are many potential targets for these signaling cascades including nuclear processes, metabolic pathways, and structural components of the cytoskeleton. There is growing appreciation of the dynamic nature of the actin cytoskeleton in smooth muscles and the necessity for actin remodeling to occur during contraction. The actin cytoskeleton serves many functions that are probably critical for muscle plasticity including generation and transmission of force vectors, determination of cell shape, and assembly of signal transduction machinery. Evidence is presented showing that actin filaments are dynamic and that actin-associated proteins comprising the contractile element and actin attachment sites are necessary for smooth muscle contraction.

Actins↗
PubMed1991

Protein engineering and the study of muscle contraction in Drosophila flight muscles.

We describe an experimental approach to the use of genetics to study muscle contraction in Drosophila melanogaster. Mutations induced by in vitro mutagenesis are inserted into the genome of flies using P-element mediated transformation, permitting the effects of the mutant genes to be studied in vivo in the indirect flight muscles (IFMs). Details of how mechanical experiments can be performed on skinned IFMs, despite their small size, are provided. The effects of two in vitro actin mutations, G368E and E316K, are described. The problems of performing biochemical and biophysical experiments on the IFMs and their myofibrillar proteins are described, together with indications as to how these may be overcome.

Actins↗
PubMed2002

Muscle contraction under capillaries in hamster muscle induces arteriolar dilatation via K(ATP) channels and nitric oxide.

We tested the hypothesis that adenosine and nitric oxide can be sensed by capillaries and are implicated in the remote arteriolar dilatation initiated by muscle contraction. We also explored a role for K(ATP) channel activity in this response. Small bundles of muscle fibres underlying a group of capillaries in cremaster muscles of anaesthetized hamsters were electrically stimulated to contract for 2 min at each of 2, 4 and 8 Hz. Diameter changes were measured in the inflow arteriole to the group of capillaries after muscle contraction in the presence or absence of 10(-6) M xanthine amine congener (XAC) to block A(1) and A(2) adenosine receptors, 10(-4) or 10(-3) M N(omega)-nitro-L-arginine (LNNA) to block nitric oxide production, or 10(-5) M glibenclamide to block K(ATP) channel activity. Dilatations were unchanged with XAC (3.0 +/- 0.5, 3.9 +/- 0.7 and 6.1 +/- 1.0 microm), but were significantly reduced with LNNA (to 1.8 +/- 0.6, 3.5 +/- 0.7 and 4.9 +/- 0.7 microm) or glibenclamide (to 0.4 +/- 0.3, 0.8 +/- 0.7 and 1.9 +/- 0.6 microm). Neither K(ATP) channel activity nor nitric oxide was required for transmission or manifestation of the dilator response. Thus, muscle contraction can be sensed by capillaries and the signalling mechanism for the ensuing remote dilatation depends on K(ATP) channel activity and on NO, but not adenosine. Local application of 10(-4) M adenosine, 10(-4) M sodium nitroprusside or 10(-5) M pinacidil directly to capillaries initiated remote arteriolar dilatations. Thus, capillaries can respond directly to known mediators of metabolic vasodilatation, but these signalling pathways are not invariably implicated in the response to muscle contraction.

ATP-Binding Cassette Transporters↗
PubMed2002

Nitric oxide synthase (NOS) coexists with activated neurons by skeletal muscle contraction in the brainstem of cats.

Contraction of skeletal muscle evokes increases in arterial blood pressure and heart rate. Some regions of the brainstem have been implicated for expression of the cardiovascular responses to muscle contraction. Previous studies have reported that static muscle contraction induced c-Fos protein in the nucleus of tractus solitarii (NTS), lateral reticular nucleus (LRN), lateral tegmental field (FTL), subretrofacial nucleus (SRF), A1 region and periaqueductal gray (PAG) of the brainstem. Furthermore, neuronal NADPH-diaphorase (NADPH-d), which is considered as a marker of neuronal nitric oxide synthase (nNOS), has been localized in those same regions. In this study, static muscle contraction was induced by electrical stimulation of the L7 and S1 ventral roots in anaesthetized cats. Distribution of c-Fos protein within neurons containing nNOS was evaluated by double labeling methods in order to determine if nNOS containing neurons in the brainstem were activated during muscle contraction. The results indicate that c-Fos protein colocalized with NADPH-d positive staining within the neurons of the SRF and PAG, but not within the NTS neurons. Distinct number of neurons with c-Fos protein was in close proximity to NADPH-d positive staining in the NTS, SRF, and PAG. Coexisting of c-Fos protein and NADPH-d positive staining was not observed in the LRN, FTL and A1 region. These findings demonstrate that nNOS containing neurons were activated by muscle contraction in the selective regions of the brainstem, and nNOS positive staining had close anatomic contacts with the neurons activated by contraction. This result provides neuroanatomic evidence suggesting that nitric oxide modulates the cardiovascular responses to muscle contraction within the NTS, SRF and PAG of the brainstem.

Anesthesia↗
PubMed2001

Simultaneous glutamate and gamma-aminobutyric acid release within ventrolateral medulla during skeletal muscle contraction in intact and barodenervated rats.

The purpose of this study was to determine if baroreflex modulates cardiovascular responses and neurotransmitter release within rostral (RVLM) and caudal (CVLM) ventrolateral medulla during static contraction of skeletal muscle using anesthetized rats. We evoked cardiovascular responses by a static muscle contraction and measured simultaneous release of glutamate and gamma-aminobutyric acid (GABA) in both the RVLM and CVLM using microdialysis probes, two inserted bilaterally into the RVLM and two into the CVLM. In intact anesthetized rats, a muscle contraction increased release of glutamate concomitantly in both the RVLM and CVLM along with significant increases in heart rate and arterial blood pressure. In contrast, concentrations of GABA increased within the RVLM, but decreased significantly within the CVLM during the pressor response. These changes were due to contraction-evoked activation of muscle afferents since tibial nerve stimulation following muscle paralysis failed to evoke glutamate, GABA, or any cardiovascular changes. On the other hand, static muscle contractions in baroreceptor denervated rats augmented the increases in heart rate and blood pressure. Furthermore, muscle contraction significantly enhanced the release of glutamate in the RVLM but attenuated its release in the CVLM. In addition, concentrations of GABA within the RVLM were attenuated following a muscle contraction in denervated rats without any changes in GABA within the CVLM. These results demonstrate that the baroreceptors influence cardiovascular responses to static muscle contraction associated with dynamic changes in glutamate and GABA release within the RVLM and CVLM.

Animals↗
PubMed1990

[Muscle contraction headache and posture--with special reference to ischemic contraction of the posterior neck muscles].

Cause of muscle contraction headache (MCH) results from sustained contraction of scalp and posterior neck muscles. Recently, we published an effect of posture on the etiology of MCH. According to our data, head bending posture seems to be one of the main causes of sustained contraction of the posterior neck muscles. Wolff presented a hypothesis of ischemic contraction of these muscles as a cause of pain. However, about the blood flow of scalp or posterior neck muscles, only two reports were published so far. These two papers failed to demonstrate a reduction of blood flow in MCH patients, and neglected the effect of posture. The purpose of this report is to examine a change of blood flow of posterior neck muscles with the change of posture. A total of 40 patients with MCH were studied using laser doppler blood flow meter. Needle shaped probe with a diameter of 0.55 mm was inserted 15 mm into the posterior neck muscle. The angle between orbito-meatal line and horizontal plane were measured using a light helmet with goniometer. Surface EMG of the posterior neck muscles was recorded at the same time. In the case of controls who do not experience headache, the amplitude of EMG increases slightly with the bending posture (40 microV with OM line 20 degrees upward from the horizontal plane, 46 microV with OM line horizontal, and 52 microV when 30 degrees downward). In reverse to the increase of the EMG activity, blood flow of the neck muscles decreases (12 ml/100 g/min with OM line 20 degrees upward, 10.8 with OM line horizontal, 7.6 at 10 degrees down, 4.6 at 20 degrees down, and 4.1 at 30 degrees down).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Gastrointestinal longitudinal muscle contractions.

The patterns of longitudinal muscle contractions of the stomach and the small intestine and their relationship with circular muscle contractions during the fasting and the fed state were investigated in conscious dogs. In the stomach, the longitudinal muscle contracted in a 1:1 relationship with the circular muscle contractions. There was no significant difference between the frequency, duration, and time of onset of gastric longitudinal and circular muscle contractions, and their amplitudes were significantly correlated with each other. In the small intestine when the circular muscle contracted, the longitudinal muscle exhibited passive elongation during the fasting and the fed state. There was no significant difference between the onset, duration, and frequency of small intestinal circular muscle contractions and the passive longitudinal muscle elongations; their amplitudes were strongly correlated with each other. During a circular muscle giant migrating contraction, the longitudinal muscle exhibited a monophasic contraction, initially a contraction followed by passive elongation or a pure passive elongation. During a retrograde giant contraction, the longitudinal muscle exhibited only a pure monophasic contraction or a contraction-elongation complex. These data suggest that the enteric nerves in the small intestine innervate the two muscle layers in a reciprocal fashion and those in the stomach in a complementary fashion.

Animals↗
PubMed2000

Smooth-muscle contraction without smooth-muscle myosin.

Here we have used gene-targeting to eliminate expression of smooth-muscle myosin heavy chain. Elimination of this gene does not affect expression of non-muscle myosin heavy chain, and knockout individuals typically survive for three days. Prolonged activation, by KCl depolarisation, of intact bladder preparations from wild-type neonatal mice produces an initial transient state (phase 1) of high force generation and maximal shortening velocity, which is followed by a sustained state (phase 2) characterized by low force generation and maximal shortening velocity. Similar preparations from knockout neonatal mice do not undergo phase 1, but exhibit a normal phase 2. We propose that, in neonatal smooth muscle phase 1 is generated by recruitment of smooth-muscle myosin heavy chain, whereas phase 2 can be generated by activation of non-muscle myosin heavy chain. We conclude that phase 1 becomes indispensable for survival and normal growth soon after birth, particularly for functions such as homeostasis and circulation.

Animals↗
PubMed2005

Effects of stretching stress on the muscle contraction proteins of skeletal muscle myoblasts.

Several studies have reported that growth and differentiation of cultured myoblasts can be facilitated by applying appropriate mechanical stimulus. However, the effects of mechanical stimulus on the characteristics of muscle fibers have not yet been fully elucidated. In this study, we gave mechanical stress to C2C12 cells, which were myoblasts derived from mice skeletal muscle. The following myosin heavy chain (MHC) isoforms were investigated in order to clarify muscle characteristics: MHC-2b, 2d and 2a, all of which are fast-twitch fibers. After inoculating cells on a silicone chamber, the chamber was mechanically stretched, and a LightCycler was used to measure the mRNA expression of each MHC isoform at several times. The results showed that, with mechanical stretching, the expression of MHC-2b was initially high. On the other hand, without stretching, the expression of MHC-2d increased over time, but with stretching, it was hardly seen. Furthermore, the expression of MHC-2a was significantly high in the stretching group. These results of this study suggest that, when intermittently stimulated, myoblasts express increased levels of MHC-2a isoform. Therefore, it is indicated that myocytes respond to environmental changes not only to facilitate growth and differentiation, but also to alter muscle function actively at the MHC isoform level.

Animals↗