Abstract
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 μM) 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.
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