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Calyculin-A inhibits nitrergic relaxations of the mouse anococcygeus

Research output: Contribution to journalArticle

A Gibson, P Wallace, I McFadzean

Original languageEnglish
Pages (from-to)213 - 215
Number of pages3
JournalEuropean Journal of Pharmacology
Issue number3
Publication statusPublished - 27 Jun 2003

King's Authors


The aim was to determine whether blockade of store-operated Ca2+ entry, or inhibition of Ca2+ 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 Ca2+ ATPase blocking agent thapsigargin (100 nM), known to prevent nitric-oxide- induced inhibition of store-operated Ca2+ entry. Conversely, the myosin phosphatase inhibitor calyculin-A (1 muM) caused almost complete abolition of nitrergic relaxations. The results provide evidence that inhibition of Ca2+ sensitisation is the major cellular mechanism underlying nitrergic relaxation of the mouse anococcygeus. (C) 2003 Elsevier Science B.V. All rights reserved.

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