PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Muscle Contraction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed2005

Effects of repeated antigen exposure on endothelin-1-induced bronchial smooth muscle contraction and activation of RhoA in sensitized rats.

Changes in endothelin-1 (ET-1)-induced contraction and activation of RhoA in bronchial smooth muscle of repeatedly antigen-challenged rats, which exhibit marked airway hyperresponsiveness (AHR), were examined. The ET-1-induced contraction of bronchial smooth muscle was significantly enhanced in the repeatedly antigen-challenged group. In normal control animals, ET-1 induced time- and concentration-dependent translocation of RhoA to the plasma membrane, indicating activation of RhoA by ET-1 in rat bronchial smooth muscle. The level of ET-1-induced RhoA translocation was increased much more markedly in the AHR group than in the control animals. It is suggested that the augmented activation of RhoA observed in the hyperresponsive bronchial smooth muscle might be responsible for the enhanced ET-1-induced contraction of bronchial smooth muscle in AHR rats.

Amides↗
PubMed2005

Comparison of brain activation after sustained non-fatiguing and fatiguing muscle contraction: a positron emission tomography study.

The concept of fatigue refers to a class of acute effects that can impair motor performance, and not to a single mechanism. A great deal is known about the peripheral mechanisms underlying the process of fatigue, but our knowledge of the roles of the central structures in that process is still very limited. During fatigue, it has been shown that peripheral apparatus is capable of generating adequate force while central structures become insufficient/sub-optimal in driving them. This is known as central fatigue, and it can vary between muscles and different tasks. Fatigue induced by submaximal isometric contraction may have a greater central component than fatigue induced by prolonged maximal efforts. We studied the changes in regional cerebral blood flow (rCBF) of brain structures after sustained isometric muscle contractions of different submaximal force levels and of different durations, and compared them with the conditions observed when the sustained muscle contraction becomes fatiguing. Changes in cortical activity, as indicated by changes in rCBF, were measured using positron emission tomography (PET). Twelve subjects were studied under four conditions: (1) rest condition; (2) contraction of the m. biceps brachii at 30% of MVC, sustained for 60 s; (3) contraction at 30% of MVC, sustained for 120 s, and; (4) contraction at 50% of MVC, sustained for 120 s. The level of rCBF in the activated cortical areas gradually increased with the level and duration of muscle contraction. The fatiguing condition was associated with predominantly contralateral activation of the primary motor (MI) and the primary and secondary somatosensory areas (SI and SII), the somatosensory association area (SAA), and the temporal areas AA and AI. The supplementary motor area (SMA) and the cingula were activated bilaterally. The results show increased cortical activation, confirming that increased effort aimed at maintaining force in muscle fatigue is associated with increased activation of cortical neurons. At the same time, the activation spread to several cortical areas and probably reflects changes in both excitatory and inhibitory cortical circuits. It is suggested that further studies aimed at controlling afferent input from the muscle during fatigue may allow a more precise examination of the roles of each particular region involved in the processing of muscle fatigue.

Adult↗
PubMed1987

The amino acid sequence of a smooth muscle-contracting peptide from chicken rectum. Identity to chicken neurotensin.

Previous studies have demonstrated that chicken rectum contains a peptide which exerts a potent, excitatory action on the smooth muscle of chicken rectum, and this peptide is most likely to be chicken neurotensin isolated recently from chicken small intestine. In the present study, the peptide was extracted from 2 kg of chicken rectums, and then it was isolated by gel filtration, ion exchange chromatography, high voltage paper electrophoresis and HPLC. Amino acid analysis of the peptide revealed that it is a tridecapeptide composed of aspartic acid (Asp), glutamic acid (Glu), proline (Pro), alanine (Ala), valine (Val), isoleucine (Ile), two residues of leucine (Leu), tyrosine (Tyr), histidine (His), lysine (Lys) and two residues of arginine (Arg). Its amino acid sequence was determined to be pGlu-Leu-His-Val-Asn-Lys-Ala-Arg-Arg-Pro-Tyr-Ile-Leu-OH. The molecule is identical to chicken neurotensin.

Amino Acid Sequence↗
PubMed2005

Role of contractile prostaglandins and Rho-kinase in growth factor-induced airway smooth muscle contraction.

BACKGROUND: In addition to their proliferative and differentiating effects, several growth factors are capable of inducing a sustained airway smooth muscle (ASM) contraction. These contractile effects were previously found to be dependent on Rho-kinase and have also been associated with the production of eicosanoids. However, the precise mechanisms underlying growth factor-induced contraction are still unknown. In this study we investigated the role of contractile prostaglandins and Rho-kinase in growth factor-induced ASM contraction. METHODS: Growth factor-induced contractions of guinea pig open-ring tracheal preparations were studied by isometric tension measurements. The contribution of Rho-kinase, mitogen-activated protein kinase (MAPK) and cyclooxygenase (COX) to these reponses was established, using the inhibitors Y-27632 (1 microM), U-0126 (3 microM) and indomethacin (3 microM), respectively. The Rho-kinase dependency of contractions induced by exogenously applied prostaglandin F2alpha (PGF2alpha) and prostaglandin E2 (PGE2) was also studied. In addition, the effects of the selective FP-receptor antagonist AL-8810 (10 microM) and the selective EP1-antagonist AH-6809 (10 microM) on growth factor-induced contractions were investigated, both in intact and epithelium-denuded preparations. Growth factor-induced PGF2alpha-and PGE2-release in the absence and presence of Y-27632, U-0126 and indomethacin, was assessed by an ELISA-assay. RESULTS: Epidermal growth factor (EGF)-and platelet-derived growth factor (PDGF)-induced contractions of guinea pig tracheal smooth muscle preparations were dependent on Rho-kinase, MAPK and COX. Interestingly, growth factor-induced PGF2alpha-and PGE2-release from tracheal rings was significantly reduced by U-0126 and indomethacin, but not by Y-27632. Also, PGF2alpha-and PGE2-induced ASM contractions were largely dependent on Rho-kinase, in contrast to other contractile agonists like histamine. The FP-receptor antagonist AL-8810 (10 microM) significantly reduced (approximately 50 %) and the EP1-antagonist AH-6809 (10 microM) abrogated growth factor-induced contractions, similarly in intact and epithelium-denuded preparations. CONCLUSION: The results indicate that growth factors induce ASM contraction through contractile prostaglandins - not derived from the epithelium - which in turn rely on Rho-kinase for their contractile effects.

Animals↗
PubMed2006

Experimental gastric dysrhythmias and its correlation with in vivo gastric muscle contractions.

AIM: To study the direct correlation between gastric dysrhythmias and in vivo gastric muscle tone. METHODS: Five healthy dogs were implanted with 4 pairs of electrodes along the greater curvature, with a strain gauge (SG) being sutured parallel to the distal electrodes (2 cm above the pylorus). Intravenous vasopressin was given to induce gastric dysrhythmia. The percentage of regular slow waves and SG energy were calculated. RESULTS: (1) the regularity of gastric myoelectric activity (GMA) was reduced during and after infusion of vasopressin; (2) SG energy was significantly decreased during the infusion of vasopressin; (3) the decrease in SG energy was well correlated with the reduction in GMA regularity; (4) SG energy was negatively correlated with bradygastria and tachygastria. CONCLUSION: Vasopressin inhibits gastric contractions and impairs gastric slow waves; gastric dysrhythmias are associated with the reduced antral muscle contractions, and are indicative of antral hypomotility.

Animals↗
PubMed1991

Vascular smooth muscle contraction and relaxation: pathways and chemical modulation.

The purpose of this review has been to summarize the information learned in the past few years regarding the mechanisms responsible for smooth muscle contraction and relaxation and to relate this information to the vasoconstrictor and vasodilator agents used by the interventional radiologist. Because this review can only provide an overview of what is known about these processes, the reader is directed to the references cited below. This reference list contains review articles that will provide in-depth information about the topics presented herein.

Endothelium, Vascular↗
PubMed1989

Altered smooth muscle contraction and sodium pump activity in the inflamed rat intestine.

We examined changes in membrane function underlying the increased contractility of jejunal longitudinal muscle to carbachol in rats infected 6 days previously with Trichinella spiralis. Muscarinic receptor characteristics were examined in particulate fractions using [N-methyl-3H]scopolamine (NMS). There was a significant reduction in the total number of binding sites on muscle from infected rats, but the affinity for NMS was unchanged. Similarly, in competition studies, the binding of carbachol to high or low affinity sites was not significantly different in tissue from control or infected rats. However, we observed an 89% suppression of the activity of K+ -stimulated ouabain-sensitive p-nitrophenylphosphatase (pNPPase), an enzyme marker for the Na+ -K+ pump, in plasma membranes from infected compared with control rats. Similar results were obtained in 86Rb uptake studies. In contractility studies, evidence for the electrogenicity of the Na+ -K+ pump was obtained by demonstrating that pump activation by K+, Rb+, or Cs+ was associated with tissue relaxation with a rank order of potency that was identical to that for stimulation of pNPPase activity by these ions. Conversely, pump inhibition by vanadate increased tone and abolished phasic contractions in muscle from control or infected rats. This was accompanied by an increased response to carbachol in muscle from control but not infected rats. In addition, pump inhibition by removing extracellular K increased tone in control tissue but decreased tone in muscle from T. spiralis-infected rats, presumably because of preexisting pump suppression. These results are consistent with the hypothesis that suppression of electrogenic Na-pump activity contributes to the increased contractility of jejunal muscle in rats infected with T. spiralis.

Animals↗
PubMed1996

Protective effect of heparin on immunologically induced tracheal smooth muscle contraction in vitro.

Our previous studies have shown that heparin, a competitive inhibitor of inositol triphosphate receptors, inhibits airway anaphylaxis in vivo. In the present study, we tested the hypothesis that heparin blocks immunologically induced tracheal smooth muscle (TSM) contraction in vitro. TSM was obtained from sheep allergic to Ascaris suum antigen, and was suspended in an organ bath containing oxygenated (95% O2, 5% CO2) Krebs-Henseleit buffer at 39 degrees C. After an equilibration period, the tissues were treated with heparin dissolved in 10 microliters DMSO, at concentrations of 1, 10, or 100 U/ml (final concentration in the bath). Two types of controls were used: vehicle (10 microliters DMSO)-treated tissues and tissues treated with the anti-asthmatic nedocromil sodium (10(-5) M). After 30 min pretreatment, tissues were challenged with 10, 30 and 100 microliters of antigen. Contractions induced by antigen were expressed as percentage of the contraction elicited by the maximum effective concentration of acetylcholine (ACh, 10(-2) M). Antigen produced dose-dependent increases in tension, which were blocked by heparin and nedocromil sodium; maximal inhibition was 43 and 52%, respectively. Neither heparin nor nedocromil sodium affected the dose-response curve or the maximum response to Ach. The addition of the heparin preservative (benzyl alcohol) did not reverse ACh-induced contractions, or inhibit antigen-induced contractile responses. These results suggest that heparin blocks immunologically induced TSM contraction, without affecting the contractile response to the airway smooth muscle agonist, ACh. This action of heparin is similar to that of the anti-asthmatic nedocromil sodium and may be related to inhibition of mast cell mediator release.

Animals↗