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PubMed1982

Craniofacial development in the absence of muscle contraction.

The muscular dysgenesis (mdg) mutation in mice causes developmental arrest of myogenesis at the myotube stage. Stained and cleared skeletal preparations and histological sections of the heads of mdg/mdg and normal mouse fetuses were compared in order to determine the effects of the mutation on craniofacial morphology. Muscles of mastication were more severely affected than tongue muscles. Mutant crania had more domed vaults and slender zygomatic arches that were displaced dorsally. The posterior part of the dysgenic mandible was bent dorsally and compressed dorsoventrally. These shape changes may be the distorting effects of persistent cervical kyphosis. Measurements of camera lucida tracings indicated that the lengths of the total mandible, the angular cartilage and process, and the condylar cartilage and process were similar between mutant and control mice. However, the widths of the condylar and angular cartilages were greatly decreased in the mutants. Moreover, the cartilages of dysgenic mice showed no size increase between 18 and 20 days of gestation. The diminished cartilages presumably result from the absence of mechanical loading from prenatal muscle function. For both condylar and angular cartilages, normal muscle activity should produce compression along the long axis of the cartilage and bending/shearing perpendicular to the long axis. It is argued that these forces are more important in promoting growth in cartilage width than length, accounting for the selective reduction of widths in the dysgenic mutant.

Animals↗
PubMed1987

O2 delivery to contracting muscle during hypoxic or CO hypoxia.

The consequences of a decreased O2 supply to a contracting canine gastrocnemius muscle preparation were investigated during two forms of hypoxia: hypoxic hypoxia (HH) (n = 6) and CO hypoxia (COH) (n = 6). Muscle O2 uptake, blood flow, O2 extraction, and developed tension were measured at rest and at 1 twitch/s isometric contractions in normoxia and in hypoxia. No differences were observed between the two groups at rest. During contractions and hypoxia, however, O2 uptake decreased from the normoxic level in the COH group but not in the HH group. Blood flow increased in both groups during hypoxia, but more so in the COH group. O2 extraction increased further with hypoxia (P less than 0.05) during concentrations in the HH group but actually fell (P less than 0.05) in the COH group. The O2 uptake limitation during COH and contractions was associated with a lesser O2 extraction. The leftward shift in the oxyhemoglobin dissociation curve during COH may have impeded tissue O2 extraction. Other factors, however, such as decreased myoglobin function or perfusion heterogeneity must have contributed to the inability to utilize the O2 reserve more fully.

Animals↗
PubMed1995

Insulin inhibits dog vascular smooth muscle contraction and lowers Ca2+i by inhibiting Ca2+ influx.

Essential hypertension, obesity and non-insulin-dependent diabetes are associated with resistance to insulin-induced glucose disposal. Because physiological concentrations of insulin inhibit vascular smooth muscle (VSM) contraction in vivo, it has been proposed that resistance to insulin-induced inhibition of VSM contraction might be partly responsible for the elevated vascular resistance found in these clinical conditions. Nevertheless, it is not known how insulin inhibits contraction of normal VSM. Several workers have demonstrated that insulin attenuates the agonist-induced intracellular Ca2+ (Ca2+i) transient in VSM, although the identity of the sarcolemmal and/or sarcoplasmic reticular Ca2+ transport systems that are affected by insulin is controversial. Our laboratory has examined the effects of a physiological concentration of insulin on contraction and Ca2+ transport in cultured VSM cells from canine femoral artery. We have found that insulin inhibits agonist-induced contraction and attenuates the agonist-induced Ca2+i transient by inhibiting Ca2+ influx, but not by increasing Ca2+ efflux or inhibiting Ca2+ release from internal stores. Insulin also stimulates ouabain-sensitive 86Rb+ uptake (Na(+)-K+ pump activity) and does not inhibit VSM contraction in the presence of ouabain. Our data support the hypothesis that insulin stimulates Na(+)-K+ pump activity, resulting in hyperpolarization of the cell and decreased Ca2+ influx via voltage-operated channels.

Animals↗
PubMed2002

ERK MAP kinases regulate smooth muscle contraction in ovine uterine artery: effect of pregnancy.

The present study investigated the potential role of extracellular signal-regulated kinase (ERK) in uterine artery contraction and tested the hypothesis that pregnancy upregulated ERK-mediated function in the uterine artery. Isometric tension in response to phenylephrine (PE), serotonin (5-HT), phorbol 12,13-dibutyrate (PDBu), and KCl was measured in the ring preparation of uterine arteries obtained from nonpregnant and near-term (140 days gestation) pregnant sheep. Inhibiting ERK activation with PD-98059 did not change the KCl-evoked contraction but significantly inhibited the contraction to 5-HT in both nonpregnant and pregnant uterine arteries. PD-98059 did not affect PE-induced contraction in the uterine arteries of nonpregnant sheep but significantly decreased it in the uterine arteries of pregnant sheep. In accordance, PE stimulated activation of ERK in uterine arteries of pregnant sheep, which was blocked by PD-98059. PD-98059-mediated inhibition of the PE-induced contraction was associated with a decrease in both intracellular Ca(2+) concentration and Ca(2+) sensitivity of contractile proteins in the uterine arteries of pregnant sheep. PDBu-mediated contraction was significantly less in pregnant than in nonpregnant uterine arteries. PD-98059 had no effect on PDBu-induced contraction in nonpregnant but significantly increased it in pregnant uterine arteries. In addition, PD-98059 significantly enhanced PDBu-stimulated protein kinase C activity. The results indicate that ERK plays an important role in the regulation of uterine artery contractility, and its effect is agonist dependent. More importantly, pregnancy selectively enhances the role of ERK in alpha(1)-adrenoceptor-mediated contractions and its effect in suppressing protein kinase C-mediated contraction in the uterine artery.

Animals↗
PubMed1985

Increases in muscle Ca2+ mediate changes in acetylcholinesterase and acetylcholine receptors caused by muscle contraction.

The synthesis of acetylcholinesterase (AcChoE; acetylcholine acetylhydrolase, EC 3.1.1.7) and of acetylcholine receptors (AcChoR) by cultured rat muscle fibers is influenced strongly by the level of muscle contractile activity. If fibers are grown in the presence of tetrodotoxin (TTX) to block spontaneous contraction, the total amount of AcChoE decreases markedly, as does the percentage of AcChoE assembled as the collagen-tailed presumed synaptic form of the enzyme. Under these conditions, however, the number of AcChoR increases. We demonstrate here that each effect of TTX can be prevented by treating the muscle cells with the calcium ionophore A23187. Thus, cells treated with A23187 and TTX have 30- to 40-fold higher levels of collagen-tailed AcChoE and lower levels of AcChoR by a factor of 4-5 than do cells grown in TTX alone. These results suggest that an increase in muscle cytoplasmic Ca2+ mediates the known effects of muscle contraction on these cholinergic macromolecules.

Acetylcholinesterase↗
PubMed1984

Limulus striated muscle provides an unusual model for muscle contraction.

Although nearly two decades have passed since de Villafranca (1961) described A-band shortening, controversy persists. Here we will review the data which has been amassed since de Villafranca 's description. We will conclude that A-bands and thick filaments shorten during sarcomere shortening in Limulus striated muscle. Further we will suggest that two machines operate in this muscle: a tension generating sliding filament system and a tension generating thick filament shortening system. Also we will suggest a mechanism of force generation of the filament shortening system and provide evidence for a cycling bridge mechanism for this muscle.

Animals↗
PubMed1980

Oxygen and vascular smooth muscle contraction revisited.

The relationship between oxygen pressure measured in a tissue bath (PBO2) and the contractile tension produced by an agonist (contractile responsiveness) was studied in a series of experiments using helical strips cut from thoracic aortas, femoral and deep femoral arteries, and small arteries taken from red and white skeletal muscle of the rabbit. The wall thicknesses of these samples ranged from 200 micron for aortas down to approximately 20 micron for the smallest skeletal muscle arteries. Contractile responsiveness of all samples became progressively depressed when PBO2 was reduced stepwise. The depression produced in the large thick-walled samples occurred at higher PBO2 levels than that produced in the small thin-walled samples. Responsiveness of all of the artery samples was depressed by hypoxia more at low than at high levels of stimulation. In a second series of experiments PO2 at the surface of artery samples (PSO2) was measured using an oxygen-sensitive microelectrode. These measurements in conjunction with calculations of the PO2 within the arterial wall (PWO2) indicated that contractile responsiveness of both large and small artery samples became depressed when PWO2 fell below a lowest-value estimate of 50 Torr. From these findings it is concluded that 1) the sensitivity of vascular smooth muscle cells to hypoxia is similar for large and small arteries; 2) this sensitivity occurs in a range of PO2 that is physiologic for resistance vessels in situ; and 3) this sensitivity to hypoxia cannot be explained by an anoxic core hypothesis and may or may not involve restricted energy metabolism.

Animals↗
PubMedDate not supplied

Transmission of acoustic or vibratory signals from a contracting muscle to relatively distant tissues.

In 20 normal subjects, acoustic or vibratory signals generated during sustained voluntary isometric contraction of the biceps brachii muscle were recorded directly over the muscle belly. The signals were also recorded simultaneously at a distance from the contracting biceps muscle over the posterior upper arm near the triceps muscle. Frequency amplitude spectra (FAS) of the recordings were determined. The amount of transmission of the most dominant vibratory signal from the biceps muscle to the posterior arm was estimated from the amplitude ratio of similar frequency peaks in the FAS obtained from recordings in these two separate regions. The mean amplitude ratio was 0.46. This finding suggests that when several groups of muscles are contracting simultaneously, there may be significant transmissions of acoustic signals from one muscle to the other. These transmissions could potentially interfere with the selective recording of sounds produced by a specific muscle.

Adult↗
PubMed2001

Combined effects of troglitazone and muscle contraction on insulin sensitization in Balb-c mouse muscle.

Thiazolidinediones, represented by troglitazone, are insulin-sensitizing agents with proven efficacy for the treatment of type 2 diabetes. Exercise is also recommended for patients with type 2 diabetes because it both stimulates glucose uptake directly and it increases insulin sensitivity following exercise. The purpose of this study was to investigate the effects of troglitazone combined with exercise on 2-deoxyglucose (2DG) uptake in both the epitrochlearis and soleus muscle of Balb-c mice. Acute, 1-h treatment with troglitazone (10 or 20 microM), in the presence or absence of insulin, had no effect on 2DG uptake in either muscle. Chronic treatment with troglitazone by feeding enhanced the insulin sensitivity and responsiveness of 2DG uptake primarily in the epitrochlearis. Direct electrical stimulation of in situ muscle was used to model exercise while the contralateral muscle was used as the unexercised control. This model mimicked exercise in that glycogen was depleted, immediate 2DG uptake was enhanced, and there was a post-exercise increase in insulin sensitivity. Troglitazone feeding had no effect on 2DG uptake in the soleus when measured immediately after electrical stimultion. However, 2DG uptake in the unstimulated epitrochlearis from troglitazone-fed mice was elevated when measured immediately after removal such that no additional effects of the electrical stimulation were measured. We found that the insulin-sensitizing effect of troglitazone was not additive to the insulin-sensitizing effect of exercise, which suggests that troglitazone and exercise share similar pathways. A unique finding in this study was the differential response to troglitazone between the epitrochlearis (fast twitch) and the soleus (slow twitch) muscle types. Possible mechanisms are discussed.

Animals↗
PubMed1967

Polarized light observations on striated muscle contraction in a mite.

Contraction of individual sarcomeres within the living mite Tarsonemus sp. was observed by polarized light microscopy. In unflattened animals the usual range of contraction was such that the minimum sarcomere length approximated the length of the A region, and the maximum sarcomere length was about twice the length of the A region. The central sarcomeres of the dorsal metapodosomal muscles were observed in detail. The A band length increased slightly with increasing sarcomere length since the regression of I region length on sarcomere length had an average slope of 0.91. When the A band length in a sarcomere which was shortening was compared with the length when the same sarcomere lengthened, no significant difference was seen. The A band of each sarcomere seemed to act as a not too rigid limit to further shortening; this agreed with the reversible shortening of a muscle in which the A band had been experimentally shortened. An H region was visible at long sarcomere lengths and was not visible at short sarcomere lengths, even when the muscle was actively shortening. The rate of change of H region length with sarcomere length suggested that I filament length may increase as sarcomere length increases. Despite this effect and the small increase in A length with sarcomere length, the results are considered to be consistent with a model in which shortening occurs by the relative movement of A and I filaments, with little or no change in length of either set of filaments. Sarcomere shortening was clearly associated with an increase in the retardation of the A region.

Animals↗
PubMed2001

Nitric oxide, reactive oxygen species, and skeletal muscle contraction.

Nitric oxide (NO) derivatives and reactive oxygen species (ROS) modulate contractile function of respiratory and limb skeletal muscle. The intracellular processes regulated by NO and ROS remain enigmatic, however. Studies of reduced preparations have identified a number of regulatory proteins that exhibit altered function when exposed to exogenous NO or ROS donors ex vivo. The relative importance of these targets in the intact cell is not known and conflicting theories abound regarding the mechanism(s) whereby NO and ROS regulate contraction. This review article provides a personal perspective on the processes regulated by NO and ROS by addressing three major topics: 1) the regulatory mechanisms by which endogenous NO depresses force production, 2) the processes whereby endogenous ROS modulate contraction of unfatigued muscle, and 3) the site(s) of action and reversibility of ROS effects in muscle fatigue.

Antioxidants↗