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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Calyculin-A inhibits nitrergic relaxations of the mouse anococcygeus.

The aim was to determine whether blockade of store-operated Ca(2+) entry, or inhibition of Ca(2+) sensitisation, is the predominant mechanism by which neuronally released nitric oxide mediates relaxation of the mouse anococcygeus. Nitrergic relaxations to field stimulation (10 Hz, 10 s trains) were unaffected by the sarcoplasmic reticulum Ca(2+) ATPase blocking agent thapsigargin (100 nM), known to prevent nitric-oxide-induced inhibition of store-operated Ca(2+) entry. Conversely, the myosin phosphatase inhibitor calyculin-A (1 microM) caused almost complete abolition of nitrergic relaxations. The results provide evidence that inhibition of Ca(2+) sensitisation is the major cellular mechanism underlying nitrergic relaxation of the mouse anococcygeus.[1]

References

  1. Calyculin-A inhibits nitrergic relaxations of the mouse anococcygeus. Gibson, A., Wallace, P., McFadzean, I. Eur. J. Pharmacol. (2003) [Pubmed]
 
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