伊比利亚毒素
BK通道
阿帕明
逼尿肌
粘菌毒素
膀胱出口梗阻
内分泌学
卡巴胆碱
化学
内科学
收缩性
钾通道
钙激活钾通道
电阻抗肌描记术
平滑肌
医学
刺激
前列腺
癌症
血管舒张
作者
Masafumi Kita,Takakazu Yunoki,Koichi Takimoto,Minoru Miyazato,Kaori Kita,William C. de Groat,Hidehiro Κakizaki,Naoki Yoshimura
出处
期刊:American Journal of Physiology-regulatory Integrative and Comparative Physiology
[American Physiological Society]
日期:2010-05-01
卷期号:298 (5): R1310-R1319
被引量:30
标识
DOI:10.1152/ajpregu.00523.2009
摘要
In this study, we investigated the effects of bladder outlet obstruction (BOO) on the expression and function of large conductance (BK) and small conductance (SK) Ca 2+ -activated K + channels in detrusor smooth muscle. The bladder from adult female Sprague-Dawley rats with 6-wk BOO were used. The mRNA expression of the BK channel α-subunit, β1-, β2-, and β4-subunits and SK1, SK2, and SK3 channels were investigated using real-time RT-PCR. All subunits except for the BK-β2, SK2, and SK3 channels were predominantly expressed in the detrusor smooth muscle rather than in the mucosa. The mRNA expression of the BK channel α-subunit was not significantly changed in obstructed bladders. However, the expression of the BK channel β1-subunit and the SK3 channel was remarkably increased in obstructed bladders. On the other hand, the expression of the BK channel β4-subunit was decreased as the severity of BOO-induced bladder overactivity progressed. In detrusor smooth muscle strips from obstructed bladders, blockade of BK channels by iberiotoxin (IbTx) or charybdotoxin (CTx) and blockade of SK channels by apamin increased the amplitude of spontaneous contractions. These blockers also increased the contractility and affinity of these strips for carbachol during cumulative applications. The facilitatory effects elicited by these K + channel blockers were larger in the strips from obstructed bladders compared with control bladders. These results suggest that long-term exposure to BOO for 6 wk enhances the function of both BK and SK types of Ca 2+ -activated K + channels in the detrusor smooth muscle to induce an inhibition of bladder contractility, which might be a compensatory mechanism to reduce BOO-induced bladder overactivity.
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