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At least 55 records · Page 3Linked to original sources
PubMed1979

Role of calcium and cyclic adenosine 3':5' monophosphate in regulating smooth muscle contraction. Mechanisms of excitation-contraction coupling in smooth muscle.

Caclium initiates smooth muscle contraction by activating an enzyme, myosin light chain kinase. This enzyme catalyzes the transfer of phosphate from adenosine triphosphate to the 20,000 dalton light chain of myosin. In its phosphorylated form myosin interacts with actin to produce muscle contraction. The mechanism by which calcium activates myosin kinase requires (1) the binding of calcium to a 16,500 dalton calcium-binding protein (calmodulin), and (2) the binding of calmodulin-calcium to a 125,000 dalton catalytic subunit. This two protein complex is the active form of myosin light chain kinase. Smooth muscle relaxation is mediated by cyclic adenosine 3':5' monophosphate (cyclic AMP). One nechanism by which the latter may exert a direct effect on actin-myosin interaction is through the activation of a cyclic AMP-dependent protein kinase that can phosphorylate the 125,000 dalton component of myosin light chain kinase. Phosphorylation of myosin light chain kinase decreases the activity of the enzyme, thus favoring the unphosphorylated form of myosin, which cannot interact with actin to produce smooth muscle contraction.

Actins↗
PubMed1969

The isolation of a substance very closely resembling the 18-monoacetate of D-aldosterone from the venous blood of activated muscle and from contracting muscle.

1. A renally active substance can be extracted in detectable quantity from 150 g flash-frozen active but not from 150 g flash-frozen flaccid striped muscle. This substance is identical to the 18-monoacetate of D-aldosterone (18-MA) in R(F) value in three solvent systems and in biological activity.2. The renally active substance is secreted into the blood stream by active but not by flaccid muscles.3. Bilateral stimulation of decentralized sciatic nerves causes diuresis, natriuresis, a rise in the clearances of creatinine and PAH without change in heart or respiratory rates, in cats under chloralose anaesthesia. These changes can be matched by I.V. infusion of ADH, 0.3-0.45 m-u./kg.min.4. The urinary changes caused by sciatic stimulation are not prevented by transection of the spinal cord but are abolished by hypophysectomy.5. Hence, like 18-MA, the muscle substance liberates ADH from the neurohypophysis.

Aldosterone↗
PubMed1998

Muscle contraction.

Understanding muscle contraction goes to the heart of one of the fundamental questions posed by classical philosophy, namely the nature of the pi nu epsilon upsilon mu alpha psi nu chi iota kappa omicron nu. The nature of 'understanding' has altered greatly during the last two millenia, particularly in response to the development of the concept of energy. Moreover, understanding contraction depends on understanding muscle structure. Galen was the first to make a detailed anatomical examination of the mode of action of muscles and recognized the heart as a muscle, but this line of research was not pursued until Leonardo da Vinci rediscovered it 1400 years later. Vesalius used the phrase Machina Carnis, but it was first Descartes who proposed a neuromuscular machine. However, the level of understanding of the physiology of muscle depends critically on the resolution of the available anatomy. Radical new insight was provided by electron microscopy. But an understanding at a physicochemical level is only possible if the structures of the components are known at atomic resolution. These have become known in the last five years and have led to dramatic progress. The present level of understanding of muscle is a physicochemical explanation of how the hydrolysis of ATP by the component proteins actin and myosin leads to movement.

Actins↗
PubMedDate not supplied

Caldesmon and thin-filament regulation of muscle contraction.

Smooth muscle contraction is regulated by phosphorylation of myosin and also possibly by the actin associated protein, caldesmon. The properties of caldesmon are discussed and compared with those of tropomyosin-troponin, the well characterized actin-based regulatory system of striated muscle. Caldesmon functions quite differently from tropomyosin-troponin. Under relaxing conditions tropomyosin-troponin does not affect the binding of myosin subfragment-1 to actin. In contrast, caldesmon strongly inhibits the binding of subfragment-1 to actin in the presence of ATP. This inhibition of binding parallels the decrease in ATPase activity that occurs as the caldesmon concentration is increased. Caldesmon has the opposite effect on the two headed myosin subfragment, heavy meromyosin. The apparent binding of skeletal heavy meromyosin increases slightly as the caldesmon concentration is increased, although the rate of ATP hydrolysis is inhibited. It is suggested that in the presence of caldesmon, myosin.ATP does not bind to the productive actin binding site but interacts with a distinct site on actin-caldesmon. This could lead to both an inhibition of ATP hydrolysis and an increase in resting stiffness of relaxed smooth muscle.

Actin Cytoskeleton↗
PubMed1986

Calcium binding to skeletal muscle troponin C and the regulation of muscle contraction.

Skeletal muscle contraction is initiated by Ca2+ ion binding to troponin C (TnC), a protein of the thin filament. Our three-dimensional structure determination of turkey skeletal TnC at 2.8 A resolution revealed an extended molecule consisting of two domains connected through a long nine-turn alpha-helix. The C-terminal domain has two Ca2+ ions bound in the expected manner of EF hands, whereas the N-terminal regulatory domain is Ca2+-free with a helix-loop-helix conformation different from that of an EF hand. The refinement of TnC at 2.2 A resolution highlights the intricate hydrogen-bonded network common to the Ca2+-bound loops and provides an explanation for the presence of a water molecule in the 5th coordination position of the Ca2+ ion. We propose that Ca2+ binding to the regulatory domain is accompanied by a conformational transition by which its structure becomes similar to that of the C-terminal domain. Dramatic movements of residues in the B and C helices and the connecting peptide of up to 14 A constitute the bulk of this change. A hydrophobic site that could be the site of interaction with troponin I is thereby exposed. We have also demonstrated that this model of the Ca2+-bound conformation can be reached from the Ca2+-free state without having to surmount large energy barriers.

Amino Acid Sequence↗
PubMed1980

The effect of insulin on skeletal muscle contractions and its relation to the effect produced by BETA-adrenoceptor stimulation.

The soleus, a slow-contracting, and the extensor digitorum longus (EDL), a fast-contracting muscle, from the guinea-pig were prepared for measurement of isometric contractions in vitro. Insulin, 2.5-55 mu/ml, caused a dose-dependent depression of twitches and subtetanic concentrations of the soleus muscle similar to and additive with that produced by the beta 2-adrenoceptor agonist, terbutaline. The effect of terbutaline but not that of insulin was blocked by propranolol. Insulin had no apparent effect on the contractions of the EDL, whereas terbutaline increased the force of contraction. When depressed by KCl, however, insulin partially restored the twitch tension in both muscles. The possible role of effects on the Na+-K+ transport is discussed.

Animals↗
PubMed1992

Changes in R-R interval at the start of muscle contraction in the decerebrate cat.

1. The effect on R-R interval of a brief hindlimb contraction, elicited by electrical stimulation of L7 ventral roots, was investigated in decerebrate cats. The first series of experiments was performed at both low and high carotid sinus pressure to vary the level of vagal tone. When carotid sinus pressure was elevated to increase vagal tone, contraction commenced 1 s later. 2. The change in R-R interval at low carotid sinus pressure was expressed as the difference between the mean of the five R-R intervals immediately preceding contraction and the mean of the last five R-R intervals at the end of a 5 s contraction. At high carotid sinus pressure, the change was expressed as the difference between the mean of the last five R-R intervals at the end of a 5 s contraction and the mean of five R-R intervals at an equivalent time after raising pressure alone. 3. Hindlimb contraction at low carotid sinus pressure produced a significant reduction in R-R interval from 359 +/- 25 (mean +/- S.E.M. n = 8) to 336 +/- 24 ms (P less than 0.005). At high carotid sinus pressure the response was enhanced with contraction producing a reduction in R-R interval from 474 +/- 45 to 419 +/- 47 ms (P less than 0.001). 4. The shortening of R-R interval produced by hindlimb contraction at high carotid sinus pressure, 55 +/- 8 ms, was significantly greater than that observed at low sinus pressure, 23 +/- 5 ms (P less than 0.001, n = 8, paired t test). This pattern of response was also seen at stimulation frequencies as low as 10 Hz. 5. In a second series of experiments, designed to determine the latency of the cardiac acceleration, the minimum latency between the onset of L7 ventral root stimulation and the end of the first shortened R-R interval was 687 +/- 29 ms (n = 5). 6. Atropine (0.4 mg kg-1, I.V.) prevented a 5 s contraction from producing any change in R-R interval. 7. These results indicate that afferent information originating from receptors in contracting muscles is responsible for producing an immediate shortening of R-R interval, which is mediated by vagal withdrawal. The possibility that the shortening of R-R interval at the start of contraction is linked to a reduction in arterial baroreceptor reflex sensitivity, possibly via inhibitory effects on neurones forming the central pathway of the baroreceptor reflex, is discussed.

Animals↗
PubMed1996

unc-68 encodes a ryanodine receptor involved in regulating C. elegans body-wall muscle contraction.

Striated muscle contraction is elicited by the release of stored calcium ions through ryanodine receptor channels in the sarcoplasmic reticulum. ryr-1 is a C. elegans ryanodine receptor homologue that is expressed in body-wall muscle cells used for locomotion. Using genetic methods, we show that ryr-1 is the previously identified locus unc-68. First, transposon-induced deletions within ryr-1 are alleles of unc-68. Second, transformation of unc-68 mutants with ryr-1 genomic DNA results in rescue of the Unc phenotype. unc-68 mutants move poorly, exhibiting an incomplete flaccid paralysis, yet have normal muscle ultrastructure. The mutants are insensitive to the paralytic effects of ryanodine, and lack detectable ryanodine-binding activity. The Unc-68 phenotype suggests that ryanodine receptors are not essential for excitation-contraction coupling in nematodes, but act to amplify a (calcium) signal that is sufficient for contraction.

Animals↗
PubMed1989

Muscle contraction (tension) headache.

Muscle contraction headache is the most common headache afflicting mankind. Acute muscle contraction headache usually presents no problem in treatment and is a self-limited condition. Chronic muscle contraction headache presents a very difficult treatment problem. Patients are often dependent on drugs and treatment usually necessitates a multimodal approach. The pathophysiology of muscle contraction headache is unknown. There is much controversy as to whether muscle contraction is the primary cause of this condition or whether muscle contraction is merely another component of this syndrome. The extensive research now going on in the field of chronic pain should help clarify the issue.

Headache↗
PubMed1989

Inhibition of the contraction of the isolated longitudinal muscle of the guinea-pig ileum by botulinum C2 toxin: evidence for a role of G/F-actin transition in smooth muscle contraction.

The effect of botulinum C2 toxin was studied on the contractions of the guinea pig ileum myenteric plexus longitudinal muscle preparation. Botulinum C2 toxin inhibited the muscle contraction induced by electrical stimulation (60 V; 0.5 ms; 0.33 Hz) in a time and concentration dependent manner. The inhibitory effect occurred with a time lag of about 1 h, and depended on the presence of both toxin components. After 4 h of incubation with 1.7 micrograms/ml of component I and 6.7 micrograms/ml of component II of botulinum C2 toxin, the smooth muscle contraction was inhibited by about 60%. At these toxin concentrations, about 55% of the modifiable smooth muscle actin was ADP-ribosylated. Smooth muscle contraction induced by bradykinin and bethanechol were similarly inhibited. Moreover, the C2 toxin inhibited muscle contraction induced by Ba2+, and by direct muscle membrane depolarization (60 V; 10 ms; 0.33 Hz) after suppression of acetylcholine release by normorphine. Also cytochalasin D inhibited the electrically evoked contraction of the ileum longitudinal muscle. In contrast to botulinum C2 toxin, inhibition of contractility by cytochalasin D occurred without a lag phase, and was reversed by washing off the toxin. In contrast of guinea pig ileum longitudinal muscle, botulinum C2 toxin did not reduce the contraction of the rabbit aortic smooth muscle stimulated by K+-depolarization or noradrenaline.

Actins↗
PubMed2001

Axial disposition of myosin heads in isometrically contracting muscles.

Meridional x-ray diffraction diagrams, recorded with high angular resolution, from muscles contracting at the plateau of isometric tension show that the myosin diffraction orders are clusters of peaks. These clusters are due to pronounced interference effects between the myosin diffracting units on either side of the M-line. A theoretical analysis based on the polarity of the myosin (and actin) filaments shows that it is possible to extract phase information from which the axial disposition of the myosin heads can be determined. The results show that each head in a crown pair has a distinct structural disposition. It appears that only one of the heads in the pair stereospecifically interacts with the thin filament at any one time.

Actins↗