Saito M, Gotoh M, Kato K, Kondo A
Department of Urology, Nagoya University School of Medicine, Japan.
J Urol. 1989 Aug;142(2 Pt 1):418-21. doi: 10.1016/s0022-5347(17)38776-1.
We investigated in vitro the supersensitivity of denervated rabbit bladder to Ca2+. Seven days after denervation achieved by bilateral sacral rhizotomy, the capacity of the denervated bladder increased by 2.2 times as compared with the control (126.3 to 277.3 ml.), and wet weight also increased 4.3 times (3.6 to 15.3 gm.). After 30 minutes incubation in normal Krebs' solution the denervated bladder strips showed significantly increased amplitude of contractions to the cumulative acetylcholine addition than the control. After incubation in normal Krebs' solution for 30 minutes, muscle strips were washed three times with Ca-free Krebs' solution and incubated 30 minutes in this solution. Cumulative Ca2+ replenishment (0.5 to 10 mM) induced dose-dependent contractions of the detrusor muscle strips in Ca2+-free Krebs' solution, where the contractions were significantly stronger in the denervated detrusor muscle than in controls. Pretreatment with 10(-6) M verapamil (Ca-entry blocker) eliminated the enhanced Ca2+-induced contractions of the denervated detrusor strips, while 10(-6) M procaine (Ca-induced Ca releasing blocker) only partially inhibited them. After depolarizing the cell membrane with 40 mM KCl, the Ca2+-induced contractions of the control strips were markedly enhanced but those of the denervated strips were not. These results demonstrate the supersensitivity of the denervated detrusor muscle to Ca2+. We conclude that hyperpermeability of the cell membrane to Ca2+ influx through calcium channels is responsible for supersensitivity of the denervated detrusor muscle to Ca2+.
我们在体外研究了去神经支配的兔膀胱对Ca2+的超敏感性。通过双侧骶神经根切断术实现去神经支配7天后，去神经支配膀胱的容量与对照组相比增加了2.2倍（从126.3毫升增至277.3毫升），湿重也增加了4.3倍（从3.6克增至15.3克）。在正常Krebs溶液中孵育30分钟后，去神经支配的膀胱条对累积添加的乙酰胆碱的收缩幅度比对照组显著增加。在正常Krebs溶液中孵育30分钟后，将肌肉条用无钙Krebs溶液洗涤三次，并在该溶液中孵育30分钟。在无钙Krebs溶液中，累积补充Ca2+（0.5至10 mM）可诱导逼尿肌条产生剂量依赖性收缩，其中去神经支配的逼尿肌收缩明显强于对照组。用10(-6)M维拉帕米（钙通道阻滞剂）预处理可消除去神经支配的逼尿肌条增强的Ca2+诱导收缩，而10(-6)M普鲁卡因（钙诱导钙释放阻滞剂）仅部分抑制它们。用40 mM KCl使细胞膜去极化后，对照组条带的Ca2+诱导收缩明显增强，但去神经支配条带的收缩未增强。这些结果证明了去神经支配的逼尿肌对Ca2+的超敏感性。我们得出结论，细胞膜对通过钙通道流入的Ca2+的高通透性是去神经支配的逼尿肌对Ca2+超敏感性的原因。
