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MeSH Review

Muscle Contraction

 
 
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Disease relevance of Muscle Contraction

 

Psychiatry related information on Muscle Contraction

 

High impact information on Muscle Contraction

 

Chemical compound and disease context of Muscle Contraction

 

Biological context of Muscle Contraction

 

Anatomical context of Muscle Contraction

 

Associations of Muscle Contraction with chemical compounds

  • In the American lobster, octopamine produces an increase in muscular tension during activation of the motor nerve and may induce spontaneous contractions at concentrations of 10(-7) M (refs 1,2) [31].
  • GABA(A) (gamma-aminobutyric acid(A)) receptors are molecular substrates for the regulation of vigilance, anxiety, muscle tension, epileptogenic activity and memory functions, which is evident from the spectrum of actions elicited by clinically effective drugs acting at their modulatory benzodiazepine-binding site [32].
  • Calcium ions activate muscle contraction [33].
  • Anxiety and muscle tension as consequences of caffeine withdrawal [34].
  • These data indicate that AMPK transmits a portion of the signal by which muscle contraction increases glucose uptake, but other AMPK-independent pathways also contribute to the response [35].
 

Gene context of Muscle Contraction

 

Analytical, diagnostic and therapeutic context of Muscle Contraction

  • GABAA receptors are molecular substrates for the regulation of vigilance, anxiety, muscle tension, epileptogenic activity, and memory functions, and the enhancement of GABAA receptor-mediated fast synaptic inhibition is the basis for the pharmacotherapy of various neurological and psychiatric disorders [41].
  • The postarteriolar response of capillary transport and microvascular flow distribution to muscle contraction and to adenosine was measured by the indicator dilution technique in isolated dog gracilis muscles perfused with blood at controlled flows [42].
  • By using as bioassay an isolated and perfused frog (Rana esculenta) heart preparation, we show here that HCNP acts on the cardiac mechanical performance exerting a negative inotropism and counteracting the adrenergic stimulation of isoproterenol [43].
  • NMR spectroscopy and selective isotope labeling of both recombinant cardiac troponin C (cTnC3) and a truncated cardiac troponin I (cTnI/NH2) lacking the N-terminal 32-amino acid cardiac-specific sequence have been used to probe protein-protein interactions central to muscle contraction [44].
  • RESULTS: Biofeedback and relaxation were associated with significant decreases in average blood glucose, A1C, and muscle tension compared with the control group [45].

References

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