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.
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 obstructionrat 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 obstructionrats, 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.