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Downregulation of TWIK‐related arachidonic acid‐activated K + channel in the spinal cord of rats after complete bladder outlet obstruction
Author(s) -
Wu Xilian,
Liang Yueyou,
Zhang Zhongyun,
Cao Mingxin,
Liang Weijie
Publication year - 2012
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.2012.03072.x
Subject(s) - bladder outlet obstruction , arachidonic acid , medicine , spinal cord , cystometry , downregulation and upregulation , western blot , urinary bladder , endocrinology , chemistry , biochemistry , prostate , cancer , psychiatry , gene , enzyme
Objectives: To study the altered expression of TWIK‐related arachidonic acid‐activated K + channel in the L6–S1 spinal cord of rats after complete bladder outlet obstruction, and to investigate the role of TWIK‐related arachidonic acid‐activated K + channel in the neurogenic mechanism of bladder dysfunction. Methods: Female Sprague–Dawley rats were randomly divided into a complete bladder outlet obstruction group and a sham‐operated control group. Cystometry was carried out and tissues of L6–S1 spinal cord were obtained for detection of TWIK‐related arachidonic acid‐activated K + channel mRNA and protein by real‐time polymerase chain reaction, western blot and immunohistochemistry. Results: The bladder outlet obstruction rat model was established. Real‐time polymerase chain reaction, western blot and immunohistochemistry showed that the expression of TWIK‐related arachidonic acid‐activated K + channel was lower in the L6–S1 spinal cord of the bladder outlet obstruction rats, compared with the control rats. Conclusions: Downregulation of TWIK‐related arachidonic acid‐activated K + channel might enhance the excitability of the neurons and increase the sensitivity of the bladder, probably providing a new study model of overactive bladder secondary to bladder outlet obstruction.