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At least 1,063 records · Page 59Linked to original sources
PubMed1990

Interactions between Ca2+ and cAMP messenger system in regulation of airway smooth muscle contraction.

Cholinergic stimuli acting via muscarinic receptors stimulate airway smooth muscle to contract and beta-adrenergic stimuli induce it to relax. Cholinergic agonists stimulate intracellular Ca2+ release and Ca2+ influx, and beta-adrenergic agonists stimulate adenosine 3',5'-cyclic monophosphate (cAMP) production. Since it was found that cAMP alters cholinergic agonist-induced changes in cellular Ca2+ metabolism, it was postulated that cAMP brought about a relaxation of this smooth muscle primarily by altering Ca2+ metabolism. More recently, it has become clear that when cholinergic agonists, as well as histamine and serotonin, act, the hydrolysis of polyphosphoinositols is stimulated, diacylglycerol production is increased, and coordinated changes in Ca2+ metabolism and protein kinase function occur. These agonists also act to inhibit adenylate cyclase activity. Conversely, it has been found that in the absence of agonist activation, cAMP increases Ca2+ influx without stimulating contraction and that in the presence of muscarinic agonists, it acts to inhibit polyphosphoinositide hydrolysis. In addition, cAMP has been shown to alter the state of phosphorylation of a number of cellular proteins, an effect that is independent of any effect on cellular Ca2+ metabolism. Based on these newer data, an expanded model of Ca2(+)-cAMP interactions in the regulation of airway smooth muscle tone is presented. A key feature of this model is the operation of dual, reciprocal inhibitory signals by which the Ca2+ and cAMP messenger systems modulate each other's expression.

Animals↗
PubMed1991

Psychophysiological parameters of migraine and muscle-contraction headaches.

Previous headache studies have been unable to verify the presumed presence of headache. Attempting to correct this design fault, the present study assessed four psychophysiological measures (frontalis EMG, temporal BVP, temporal and finger skin temperature) and salient subjective measures in 13 migraineurs, eight muscle-contraction headache sufferers, and 13 age-matched normals. All subjects submitted to two 30-minute sessions of quiet monitoring, and for the headache subjects, one of the sessions was headache active. A bogus, but convincing preliminary "assessment" revealed insufficient headache activity in the headache active session, forcing subjects to reschedule that session in the future when a strong headache was present. A parallel manipulation was employed with the normal subjects. A MANOVA failed to discriminate within- or between-group differences on the psychophysiological measures. Self-reported pain was uncorrelated with the psychophysiological indices. These results cast further doubt on the validity of the psychophysiological measures employed in this study, the same ones routinely endorsed by headache researchers and therapists. We discuss problems of recruitment, compliance, and attrition in basic headache research.

Electromyography↗
PubMed1993

Role of muscle perfusion and baroreception in the hyperpnea following muscle contraction in dog.

The influence of impeding muscle perfusion on the time course of ventilatory decline during recovery from electrically induced hindlimb contractions has been studied in 14 anesthetized dogs. When intravascular balloons, placed in abdominal aorta and inferior vena cava just rostral to the iliac bifurcation, were inflated at the cessation of contraction bout, minute ventilation (VE) was significantly reduced during recovery compared with control. The subsequent restoration of iliac circulation rapidly augmented VE, which peaked at the fifth breath after release, by an average of +4.97 L.min-1; VE then returned exponentially to resting (pre-contraction) level. Breathing 100% O2 did not affect the VE recovery pattern neither during iliac occlusion nor immediately after its release (the peak average delta VE = +4.42 L.min-1). When a local anesthetic (5% Lidocaine) was applied bilaterally to the regions of carotid bifurcation, systemic blood pressure was significantly increased and the VE response to both iliac occlusion and release were nearly abolished. The VE response to inhalation of 5% CO2 in air was not affected by this procedure, whereas the stimulation of VE with 2 mg i.v. bolus of NaCN was attenuated. When the local anesthetic was thoroughly washed out (and systemic blood pressure had returned to control level) the previously observed VE responses to iliac occlusion and release were restored. These results and analysis of the VE response timing (transits and latencies) suggest that the vascular rather than humoral effects or tissue 'metaboreception' modulate ventilatory recovery from muscular contractions; baroreception appears to be important in this process.

Animals↗
PubMed1976

[Comparison of the compliance of resting and contracting muscle].

Frog sartorius muscles are stretched at rest and during maximal tetanic contractions. Parallel compliance decreases when the length increases. The relationship between compliance and length is linear in double-logarithmic scale. The compliance of the active muscle (tetanic contraction) is not related to the length. The series-compliance is calculated from the parallel compliance and the active one. It increases with the length of muscle. These results are discussed on the basis of the sliding-filaments theory.

Animals↗
PubMed1988

Effect of amiloride on regulatory mechanisms of vascular smooth muscle contraction.

Experiments were conducted to characterize the effects of amiloride on the regulatory mechanisms of vascular smooth muscle contraction. Intact, saponin-skinned and A23187-treated strips of rabbit aorta were used for these studies. Amiloride significantly (P less than 0.05) reduced the norepinephrine bitartrate (NE)-stimulated increase in intracellular Ca2+ in intact arteries. In saponin-skinned arteries, amiloride depressed both stress and concomitant levels of myosin light chain phosphorylation. This inhibition of stress appeared to be competitive with MgATP. In A23187-treated preparations, where the effects of amiloride were studied at physiological [MgATP] in the absence of functional membrane Ca2+-channels, amiloride caused a reduction in both stress and myosin light chain phosphorylation. In other experiments on intact arteries, the contractile response to phorbol 12,13-dibutyrate, an activator of protein kinase C, was reduced by amiloride. We conclude that the vasorelaxant effects of amiloride are mediated via inhibition of myosin light chain kinase and protein kinase C, in addition to the inhibition of Ca2+ influx.

Adenosine Triphosphate↗
PubMed1976

Free energy levels and entropy production in muscle contraction and in related solution systems.

"Basic" and "gross" free energy levels of a macromolecule such as myosin or Na,K-ATPase, defined in a previous publication, are discussed here for two relatively complicated cases: a six-state kinetic diagram of the sort that could be used to describe the actin activation of myosin-ATPase in solution; and muscle contraction, where a similar kinetic diagram is needed for each value of a positional variable X.

Actins↗
PubMed2006

Phosphorylation of caldesmon during smooth muscle contraction and cell migration or proliferation.

The actin-binding protein caldesmon (CaD) exists both in smooth muscle (the heavy isoform, h-CaD) and non-muscle cells (the light isoform, l-CaD). In smooth muscles h-CaD binds to myosin and actin simultaneously and modulates the actomyosin interaction. In non-muscle cells l-CaD binds to actin and stabilizes the actin stress fibers; it may also mediate the interaction between actin and non-muscle myosins. Both h- and l-CaD are phosphorylated in vivo upon stimulation. The major phosphorylation sites of h-CaD when activated by phorbol ester are the Erk-specific sites, modification of which is attenuated by the MEK inhibitor PD98059. The same sites in l-CaD are also phosphorylated when cells are stimulated to migrate, whereas in dividing cells l-CaD is phosphorylated more extensively, presumably by cdc2 kinase. Both Erk and cdc2 are members of the MAPK family. Thus it appears that CaD is a downstream effector of the Ras signaling pathways. Significantly, the phosphorylatable serine residues shared by both CaD isoforms are in the C-terminal region that also contains the actin-binding sites. Biochemical and structural studies indicated that phosphorylation of CaD at the Erk sites is accompanied by a conformational change that partially dissociates CaD from actin. Such a structural change in h-CaD exposes the myosin-binding sites on the actin surface and allows actomyosin interactions in smooth muscles. In the case of non-muscle cells, the change in l-CaD weakens the stability of the actin filament and facilitates its disassembly. Indeed, the level of l-CaD modification correlates very well in a reciprocal manner with the level of actin stress fibers. Since both cell migration and cell division require dynamic remodeling of actin cytoskeleton that leads to cell shape changes, phosphorylation of CaD may therefore serve as a plausible means to regulate these processes. Thus CaD not only links the smooth muscle contractility and non-muscle motility, but also provides a common mechanism for the regulation of cell migration and cell proliferation.

Animals↗
PubMed2006

2-Aminoethoxydiphenyl borate inhibits KCl-induced vascular smooth muscle contraction.

K(+)-depolarization (KCl)-activated Ca(2+) entry permitting sustained force-maintenance in tonic vascular smooth muscle has long been attributed solely to activation of L-type voltage-operated Ca(2+) channels (VOCs). We used the transient receptor potential channel (TRP) blocker, 2-aminoethoxydiphenyl borate (2-APB), to test the hypothesis that KCl activates additional Ca(2+) entry pathways. 2-APB alone caused a transient weak increase in force, a sustained weak increase in basal [Ca(2+)](i) and myosin light chain phosphorylation, and inhibition of KCl-induced force, [Ca(2+)](i) and myosin light chain phosphorylation. 2-APB did not appear to block VOCs, because 2-APB did not inhibit 30 nM Bay k 8644-induced increases in [Ca(2+)](i). Moreover, although 1 microM nifedipine abolished the increase in [Ca(2+)](i) produced by alpha-adrenergic receptor activation, 2-APB produced an additional reduction in [Ca(2+)](i) below the basal level. These data support the conclusion that membrane depolarization activates 2-APB-sensitive TRPs in addition to VOCs to permit strong force-maintenance in tonic vascular smooth muscle.

Animals↗
PubMed2002

New parameters reducing the interindividual variability of metabolic changes during muscle contraction in humans. A (31)P MRS study with physiological and clinical implications.

Interindividual variations in skeletal muscle metabolism make comparative analyses difficult. In this study, we have addressed the issue of capturing the variability of metabolic performance observed during muscle exercise in humans by using an original method of normalization.Metabolic changes induced by various kinds of exercise were investigated using 31P magnetic resonance spectroscopy (MRS) at 4.7 T in 65 normal subjects (23 women and 42 men) and 12 patients with biopsy-proven muscular disorders. Large variations in the extent of PCr breakdown and intracellular acidosis were recorded among subjects and exercise protocols. For all the data pooled, the amplitude of mechanical performance accounts for 50% of these variations. When scaled to the work output, variations of PCr consumption account for 65% of pH changes through a linear relationship. This linear relationship was substantially improved (90%) when both variables were scaled to the square of work output performed (P1 and P2). By capturing most of the initial interindividual variability (90%), P1 vs. P2 relationship represents an ideal standardization procedure, independent of any anthropometric measurements. This relationship also discloses a significant link between the extent of PCr breakdown and intracellular acidosis regardless of exercise protocol. Moreover, changes in the slope of the P1 vs. P2 regression curve, as measured in old subjects and in selected patients, directly reflect alterations of energy production in muscle.

Adult↗
PubMed2002

Effects of creatine loading and depletion on rat skeletal muscle contraction.

1. In humans, the effects of dietary creatine supplementation are controversial, with some studies showing increased muscle force and fatigue resistance and others reporting no effect on exercise performance. Little is known about the effects of creatine on muscle contractile properties. 2. Rats were fed a standard diet, creatine for 10 days or beta-guanidinopropionate, which depletes muscle creatine, for 7 days. Contractile properties were measured in isolated extensor digitorum longus and sternohyoid muscle as representative limb and upper airway dilator muscles, respectively. 3. Creatine had no effect on specific twitch and tetanic tension, contractile kinetics, twitch/tetanus tension ratio, the tension-frequency relationship or fatigue in both muscles. beta-Guanidinopropionate had no effect on the twitch and tetanic tension, contractile kinetics, twitch/tetanus tension ratio or tension-frequency relationship, but significantly increased (P < 0.05, anova) fatigue in both muscles. 4. Therefore, although creatine depletion increases fatigue, creatine loading has no effects on extensor digitorum longus and sternohyoid muscle contractile properties.

Animals↗
PubMed1971

A mechanochemical mechanism for muscle contraction.

A mechanism for contraction in skeletal muscle is proposed in which the tension-generating site is located within the core of the thick (myosin) filament, specifically within the trypsin-sensitive hinge region of the myosin rod. The force-developing mechanism is thought to be the transfer of energy from ATP splitting in the globular head of one molecule directly to the hinge region of an adjoining molecule, resulting in a phase transition from crystalline to amorphous within the hinge segment of the second molecule. Binding of MgATP at the actinmyosin interface is considered to be a release mechanism. The model leads to out-of-phase oscillating movement of the cross bridges.

Adenosine Triphosphatases↗