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Results for “Muscle Contraction”

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PubMed1994

Inhibitory effect of interleukin-6 on vascular smooth muscle contraction.

Our objective was to investigate the direct effect of interleukin-6 (IL-6) on the vascular smooth muscle contraction. We measured the contraction of endothelium-denuded aortic rings isolated from Sprague-Dawley rats. We also investigated the involvement of vasodilator prostaglandin and guanosine 3',5'-cyclic monophosphate (cGMP) productions in the effect of IL-6 using cultured rat vascular smooth muscle cells (VSMC). Exposing the aortic rings to recombinant murine IL-6 (50 U/ml) for 180 min significantly suppressed the phenylephrine (10(-9)-10(-5) M)-induced contraction. This inhibitory effect of IL-6 on the contraction tended to exhibit a dose-dependent relationship (0.5-50 U/ml). The effect of IL-6 was totally eliminated in the presence of indomethacin (10(-5) M). The release of immunoreactive 6-ketoprostaglandin F1 alpha from cultured rat VSMC was significantly increased by exposure to IL-6. Intracellular cGMP concentration in VSMC was not affected by IL-6. In conclusion, IL-6 is a potent inhibitor of the alpha-adrenergic-stimulated contraction of vascular smooth muscle. Its action is endothelium independent and mediated by the increased synthesis of prostacyclin in VSMC.

Animals↗

PubMed1988

A myosin site involved in energy transduction during muscle contraction.

An antibody was developed against a 23-kDa fragment of myosin which contains a part of the ATP-binding site, and applied to skinned muscle fibers. The antibody abolished active tension generation of the fibers, but did not block their assumption of a rigor state nor their release from this state by ATP. The primary amino acid sequence of the antigenic site on the fragment was found to be the region containing residues 77-80. This sequence region is predicted to have interesting secondary structures, and is distinct from the proposed ATP-binding site. We discuss the possibility that the region is responsible for the energy-transducing step in muscle contraction.

Actins↗

PubMed1975

Catecholamine release: mechanism of mercury-induced vascular smooth muscle contraction.

The mechanism by which mercuric ion (HgCl2) induces contraction of vascular smooth muscle was defined in the kidney of anesthetized dogs and in rabbit aortic strips. In vivo, HgCl2 injected into the renal artery induced a dose-related reduction in renal blood flow (electromagnetic flowmeter) and glomerular filtration rate (creatinine clearance). An intra-arterial infusion of phenoxybenzamine (POB) significantly reduced the vascular response to HgCl2 (P less than 0.001). In vitro, alpha-adrenergic blockade with phentolamine and POB prevented mercury-induced contraction, whereas agents that block serotonin, histamine, acetylcholine, and angiotensin did not do so. Norepinephrine receptor "protection" from phenoxybenzamine blockade sustained the response to HgCl2. Reserpine pretreatment produced a parallel reduction in the response of the aorta to tyramine and mercury. The results are consistent with an indirect action of mercuric ion via release of endogenous catecholamines.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Eardrum displacement following stapedius muscle contraction.

Simultaneous monitoring in human subjects on the same ear of eardrum displacement by tympanomanometry, and impedance with the electroacoustic bridge, provided information concerning contraction of the stapedius muscle and its effect on eardrum displacement. Extensive control procedures were employed to elicit only the stapedius reflex; lower intensity auditory stimulation, electrocutaneous stimulation of the homolateral external ear canal, and anesthetization of nerves leading to the tensor tympani. Following these procedures the following results were obtained: (1) Extremely small biphasic and monophasic eardrum movements were seen in the stapedius--only ear to auditory and electrocutaneous stimulation; the form of the response was much less predictable to auditory stimulation. (2) At high sound intensities relatively large inward and biphasic movements of the eardrum occurred in the normal ear, unquestionably due to contraction of the tensor tympani. These results were further validated in a group of stapedectomized ears, without the stapedius but with normal tensor tympani. (3) Biphasic responses did not occur in the tensor tympani--only ear, only monophasic inward responses. (4) Upon air-jet stimulation to the orbit of the eye, these subjects had an accentuated tensor response in that large inward movements of the eardrum occurred as compared with those in normal ears, suggesting that there is an alteration of the tensor response by the presence of the stapedius muscle. Estimates of the actual eardrum displacement were calculated based on a model of the external ear canal and eardrum.

Acoustic Stimulation↗

PubMed2005

What limits the velocity of fast-skeletal muscle contraction in mammals?

In rat skeletal muscle the unloaded shortening velocity (Vo) is defined by the myosin isoform expressed in the muscle fibre. In 2001 we suggested that ADP release from actomyosin in solution (controlled by k(-AD)) was of the right size to limit Vo. However, to compare mechanical and solution kinetic data required a series of corrections to compensate for the differences in experimental conditions (0.5 M KCl, 22 degrees C for kinetic assays of myosin, 200 mM ionic strength, 12 degrees C to measure Vo). Here, a method was developed to prepare heavy meromyosin (HMM) from pure myosin isoforms isolated from single muscle fibres and to study k(-AD) (determined from the affinity of the acto-myosin complex for ADP, KAD) and the rate of ATP-induced acto-HMM dissociation (controlled by K1k+2) under the same experimental condition used to measure Vo). In fast-muscle myosin isolated from a wide range of mammalian muscles, k(-AD) was found to be too fast to limit Vo, whereas K1k+2 was of the right magnitude for ATP-induced dissociation of the cross-bridge to limit shortening velocity. The result was unexpected and prompted further experiments using the stopped-flow approach on myosin subfragment-1 (S1) and HMM obtained from bulk preparations of rabbit and rat muscle. These confirmed that the rate of cross-bridge dissociation by ATP limits the velocity of contraction for fast myosin II isoforms at 12 degrees C, while k(-AD) limits the velocity of slow myosin II isoforms. Extrapolating our data to 37 degrees C suggests that at physiological temperature the rate of ADP dissociation may limit Vo for both isoforms.

Adenosine Diphosphate↗

PubMed1980

A comparison of treatments for prefrontal muscle contraction headache.

A comparison of hypnotic analgesia, frontalis electromyographic feedback, and frontalis electromyographic feedback in conjunction with Jacobson progressive relaxation for treating chronic prefrontal muscle contraction headache was done. There were four 1-hour treatment sessions for each type, and a follow-up. Measures were the number of headache hours per week, a subjective estimate of pain intensity, and an objective ratio of pain intensity found by using the submaximum tourniquet technique. No significant differences were found between treatments on these dependent measures, although all produced significant change in the desired direction. The current study utilized 48 patients with chronic prefrontal headache, and was performed in a clinical situation. Certain responses to the Headache Questionnaire used in screening were significantly correlated with improvement in headache. The current study controlled for class of medication the patient may have been taking for headache, thereby giving a more realistic assessment of the effectiveness of psychological treatments in a clinic.

Biofeedback, Psychology↗

PubMed1989

Muscle contraction headache and migraine. Platelet activation and plasma norepinephrine during the cold pressor test.

For clarification of possible platelet activation in migraine and chronic muscle contraction headache (MCH) under stress, plasma platelet factor 4 (PF4), norepinephrine (NE), and free fatty acids (FFA) were investigated during the cold pressor test. Both PF4 and NE increased significantly, whereas FFA showed no remarkable changes. The increases of PF4 in MCH and migraine during this test were significantly greater than in healthy controls. The increase of PF4, however, was independent of NE increase and FFA changes. On the other hand, we observed decreased NE levels in both MCH and migraine, which might suggest peripheral sympathetic hypofunction. The platelets of MCH or migraine patients seem to be impaired, and the impairment may be caused by continuous sympathetic hypofunction. The behaviour of the above three substances in MCH was similar to that in migraine throughout the present study.

Blood Platelets↗

PubMed1995

Birth of the sliding filament concept in muscle contraction.

Why were the two classical papers by A.F. Huxley and R. Niedergerke and by H.E. Huxley and J. Hanson on the sliding filament concept in muscle contraction published in the same issue (May 22, 1954) of Nature? This historical survey reveals the background of the two groups' monumental work.

Actin Cytoskeleton↗

PubMedDate not supplied

The effects of middle ear muscle contraction on auditory and overload thresholds.

The present investigation examined psychophysically the frequency-specific and nonlinear attenuation of sound energy provided by middle ear muscle contraction in normal hearers. Aural overload and absolute auditory thresholds were measured at 500, 1 000 and 2 000 Hz prior to and during acoustic stapedial reflex contraction. Reflex contraction was elicited with contralateral broad-band noise. Results revealed that overload thresholds were elevated at 500 and 1 000 Hz and a slight decrease in overload threshold was apparent at 2 000 Hz during reflex contraction while absolute thresholds remained essentially unchanged. These data are consistent with previous psychophysical and physiological findings. The aural overload test having been derived directly from observations of cochlear microphonic saturation, moreover, affords direct comparison to results of electrophysiological experimentation.

Acoustic Stimulation↗

PubMed1986

Intracellular calcium and smooth muscle contraction.

Excitation-contraction coupling in smooth muscle involves many processes, some of which are outlined in this article. The total amount of Ca2+ released on excitation is considerably in excess of the free Ca2+ concentration and this implies a high capacity, high affinity Ca2+ buffer system. The two major Ca2+-binding proteins are calmodulin and myosin. Only calmodulin has the appropriate binding affinity to act as a component of the Ca2+-buffer system. The Ca2+-calmodulin complex activates myosin light chain kinase and thus is involved in the regulation of contractile activity. Phosphorylation of myosin stabilizes an active conformation and promotes cross bridge cycling and is essential for the initiation of contraction. During the initial contractile response phosphorylation correlates to tension development and velocity of shortening. However, as contraction continues the extent of myosin phosphorylation and velocity often decreases but tension is maintained. In general, the Ca2+ transient is reflected by the extent of phosphorylation that in turn correlates with shortening velocity. Maintenance of tension at low phosphorylation levels is not accounted for within our understanding of the phosphorylation theory and thus alternative regulatory mechanisms have been implicated. Some of the possibilities are discussed.

Animals↗

PubMed1996

Does vaginal electrical stimulation cause pelvic floor muscle contraction? A pilot study.

The purpose of the present study was to evaluate whether vaginal electrical stimulation using Conmax and Medicon MS-105 causes pelvic floor muscle contraction. In addition, pain and discomfort described by the participants were registered. Nine women, mean age 37.7 years (range 24-54) participated in the study; five healthy physio-therapists and four patients with diagnosed genuine stress incontinence. All the participants used Conmax and Medicon MS-105 with 10, 20 and 50 Hz in random order. The women increased the current step by step to tolerance level. Two physiotherapists were observing the perineum and notified whether a correct contraction was occurring. The participants reported whether there was a correct contraction of the pelvic floor and described pain and discomfort, classified according to McGill Pain Questionnaire. The results demonstrated that a correct contraction was reported and observed in only one of nine women. Electrical stimulation with all frequencies caused pain and discomfort in all women.

Adult↗

PubMed1997

Daunorubicin-induced smooth muscle contraction: involvement of Ca2+ entry mechanism.

The mechanisms of the smooth muscle contractile action of daunorubicin were investigated using guinea-pig aortae, and the involvement of the Ca2+ entry mechanism was compared among different smooth-muscle preparations. In the aorta, daunorubicin showed a concentration-dependent contractile action at concentrations of 10-200 microM. The contractile response to daunorubicin was completely dependent on extracellular Ca2+, but only slightly sensitive to verapamil or nifedipine. Trifluoperazine abolished the contraction by daunorubicin, but no significant effect was noted with amiloride, phentolamine, indomethacin or staurosporine. The order of potency (sensitivity) for daunorubicin-induced smooth muscle contraction was oesophagus = gall bladder = iliac artery > bronchus = aorta, while that of maximum reactivity was iliac artery = aorta > bronchus = oesophagus = gall bladder. In the portal vein, daunorubicin showed no contractile action. Although the smooth muscle contraction induced by daunorubicin was strongly dependent on extracellular Ca2+ in the aorta, iliac artery, bronchus, oesophagus and gall bladder, its sensitivity to verapamil varied among the different smooth muscle preparations, with the sensitivity being iliac artery = gall bladder > bronchus = oesophagus > aorta. These results suggest that daunorubicin has contractile action on various kinds of smooth muscle, mainly via the transplasmalemmal Ca2+ entry mechanism, but the degree of involvement of the voltage-dependent Ca2+ channel differs among the different smooth muscle preparations.

Animals↗

PubMed2005

Step-size of net filament sliding of muscle contraction.

The step-size defined as the movement between actin and myosin filaments per ATP split is an important issue in the research of muscle contraction. According to the conventional swinging-cross-bridge theory by Huxley, the step-size in this sense should be within 40 nm, a maximum possible stroke size of a myosin head, 20 nm, swing through an arc of 180 degrees . Since 1996, the estimated value over 40 nm has not been reported. Recently, however, there have been several discussions based on the one of the smallest values of step-size, 1.7 nm. We carefully re-evaluated the estimation process for the step-size, concluding that the values are still limited within 10-20 nm of conventional swinging-cross-bridge theory: 12.6 nm at no load for frog muscle.

Actins↗

PubMed1986

Comparative comfort of three waveforms used in electrically eliciting quadriceps femoris muscle contractions.

The purpose of this study was to compare the relative comfort levels of electrical stimulation having different waveforms, but otherwise identical current characteristics, delivered percutaneously to normal quadriceps femoris muscles contracting at the same intensity level. The quadriceps femoris muscles of 20 healthy subjects were stimulated to a torque level 60% of that obtained in a maximal voluntary isometric contraction, using pulsed current with a carrier frequency of 2,500 Hz, at 50 pulses per second of 10-msec pulse duration. Three different waveforms were used: sinusoidal, sawtooth (triangular), and square. The relative comfort level of each electrically elicited contraction for each waveform was determined for each subject using a 20-cm-long visual analog scale. The results showed that no one waveform was most comfortable (least uncomfortable) and the difference was significant in what the subjects perceived to be the most comfortable contraction, regardless of waveform (p less than .01). These results indicate that a subject's perception of discomfort changes as the waveform of stimulation varies and that individual preferences exist for different waveforms. Selection of the most comfortable waveform could prove beneficial when the intensity of muscle stimulation is increased.

Electric Stimulation↗

PubMed1988

Evaluation and management of the muscle contraction headache.

Headache was the seventh most frequent reason for a visit to primary care providers specified in the 1977-1978 National Ambulatory Care Survey. Muscle contraction headaches (MCH) constitute 90 percent of all headaches. Following a discussion of the epidemiology of headache, this article describes the pathophysiology, history, psychological profile of the typical MCH patient, common objective findings of MCH versus intracranial mass, physical findings and diagnosis. The management section includes a discussion of education and appropriate pharmacologic treatment, along with non-pharmacologic treatments such as massage, acupressure, biofeedback and stress management. Acupuncture is briefly described. Referral criteria for the MCH is included.

Acupuncture Therapy↗

PubMed1976

[Influence of homologous n-alkanoic acids on functional properties of isolated skeletal muscles. I. Muscle contraction].

1. The contractility of isolated muscles of the frog (and in some instances of the rat) was investigated at room temperature in Ringer's solutions containing homologous alkanoic acids (100 mM C4 to 0.4 mM C10). 2. Free fatty acids decrease the contraction amplitudes evoked by direct stimulation. The effects increase with concentration, exposure, and chain length of the fatty acids. In Ringer's solution the changes are totally or partly reversible. 3. The depression of contraction amplitude induced by free fatty acids is removed by small concentrations of caffeine (2--5 mM) in Ringer's solution. 4. Interactions of fatty acids with different structures of skeletal muscle (mitochondria, sarcolemma and membranes of sarcoplasmic vesicles) are discussed. The distinct effect of fatty acids on stimulated muscles and the importance of membranes in the regulation of the calcium ion concentration in the cytoplasm suggest that fatty acids interact with membrane lipids.

Alkanes↗

PubMed2000

Sustained muscle contraction induced by agonists, growth factors, and Ca(2+) mediated by distinct PKC isozymes.

The role of protein kinase C (PKC) in sustained contraction was examined in intestinal circular and longitudinal muscle cells. Initial contraction induced by agonists (CCK-8 and neuromedin C) was abolished by 1) inhibitors of Ca(2+) mobilization (neomycin and dimethyleicosadienoic acid), 2) calmidazolium, and 3) myosin light chain (MLC) kinase (MLCK) inhibitor KT-5926. In contrast, sustained contraction was not affected by these inhibitors but was abolished by 1) the PKC inhibitors chelerythrine and calphostin C, 2) PKC-epsilon antibody, and 3) a pseudosubstrate PKC-epsilon inhibitor. GDPbetaS abolished both initial and sustained contraction, whereas a Galpha(q/11) antibody inhibited only initial contraction, implying that sustained contraction was dependent on activation of a distinct G protein. Sustained contraction induced by epidermal growth factor was inhibited by calphostin C, PKC-alpha,beta,gamma antibody, and a pseudosubstrate PKC-alpha inhibitor. Ca(2+) (0.4 microM) induced an initial contraction in permeabilized muscle cells that was blocked by calmodulin and MLCK inhibitors and a sustained contraction that was blocked by calphostin C and a PKC-alpha,beta,gamma antibody. Thus initial contraction induced by Ca(2+), agonists, and growth factors is mediated by MLCK, whereas sustained contraction is mediated by specific Ca(2+)-dependent and -independent PKC isozymes. G protein-coupled receptors are linked to PKC activation via distinct G proteins.

Alkaloids↗

PubMed1996

Mechanisms of smooth muscle contraction.

Work performed with differentiated contractile smooth muscle tissue over the last two decades has made clear that covalent modification of myosin by phosphorylation of the 20-kDa myosin light chains is a significant mode of regulation of contractile activity in smooth muscle, particularly in regard to the generation of phasic contractions and the initial development of tonic contractions. This regulatory mechanism appears to be of unique importance in smooth muscle compared with striated muscle. It is equally clear, however, that there is an important role for protein kinase C in the regulation of smooth muscle tone maintenance, particularly in vascular smooth muscle. Several possible signal transduction cascades involving protein kinase C are outlined. Increasing evidence suggests a link between protein kinase C and actin-based regulatory mechanisms. This review places emphasis on relating up-to-date biochemical facts to the physiological realities of the smooth muscle cell.

Animals↗