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MeSH Review

Isometric Contraction

 
 
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Disease relevance of Isometric Contraction

 

High impact information on Isometric Contraction

  • During half-maximal isometric contraction of the tissues with acetylcholine, relaxation responses to isoproterenol, PGE2, and forskolin were separately compared in control (untreated) TSM and tissues incubated for 18 h with IL-1beta (10 ng/ml), TNF-(alpha (100 ng/ml), or IL-2 (200 ng/ml) [6].
  • METHODS: Isometric contractions of endothelium-denuded vessel rings were induced cumulatively by methoxamine and relaxations by isoproterenol [7].
  • The effect of DHEA appears to involve a large conductance Ca2+-activated potassium channel (BKCa)-dependent stimulatory mechanism, at both function and expression levels (isometric contraction and Western blot), via a redox-dependent pathway [8].
  • S100A1 gene transfer resulted in a significant increase of unloaded shortening and isometric contraction in isolated cardiomyocytes and engineered heart tissues, respectively [9].
  • Thus, isometric contraction activates eNOS via a Ca2+-independent, tyrosine kinase inhibitor-sensitive pathway and, like shear stress, seems to be an independent determinant of mechanically induced NO formation [10].
 

Chemical compound and disease context of Isometric Contraction

 

Biological context of Isometric Contraction

 

Anatomical context of Isometric Contraction

 

Associations of Isometric Contraction with chemical compounds

 

Gene context of Isometric Contraction

 

Analytical, diagnostic and therapeutic context of Isometric Contraction

References

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