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Calyculin-A inhibits nitrergic relaxations of the mouse anococcygeus.

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 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.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Gibson A,Wallace P,McFadzean I

doi

10.1016/s0014-2999(03)01866-1

keywords:

subject

Has Abstract

pub_date

2003-06-27 00:00:00

pages

213-5

issue

3

eissn

0014-2999

issn

1879-0712

pii

S0014299903018661

journal_volume

471

pub_type

杂志文章

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