Besarani Dler, Wu Changhao, Fry Christopher H
Institute of Urology, University College London, London, UK.
BJU Int. 2006 May;97(5):1083-6. doi: 10.1111/j.1464-410X.2006.06061.x.
To determine the role of Na+-Ca2+ exchange in the regulation of isolated detrusor smooth muscle contractility.
Isolated guinea-pig detrusor strips were used to record isometric tension generated by; (a) electrical-field stimulation to elicit nerve-mediated responses; and (b) adding carbachol or superfusing with a high-K+ solution. The [Na+] gradient between extracellular and intracellular compartments was altered by: (i) reducing superfusate [Na+] in stages from 140.2 to 10.2 mm; (ii) addition of the cardiac glycoside strophanthidin (200 microm). RESULTS Reducing extracellular [Na+] reversibly reduced the magnitude of nerve-mediated contractions but increased the resting tension and magnitude of carbachol-induced contracture. The mean (sd) [Na+] required for a half-maximum effect on attenuating contractions, at 85.9 (6.2) mm, and developing contracture, at 59.1 (14.3) mm, were significantly different. The time constants of changes to nerve-mediated contractions and carbachol contracture were also significantly different, at 147 (5) vs 1207 (386) s, respectively. These differences suggest that separate mechanisms influence nerve-mediated contraction and contracture in low-Na+ solutions. Exposure to the cardiac glycoside strophanthidin produced a similar effect to low-Na+ solutions for carbachol contracture. Low-Na+ solutions had no significant effect on contractures induced by high extracellular [K+]. CONCLUSION Reducing the transmembrane [Na+] difference increases intracellular [Ca2+]. This increase is largely accommodated in intracellular stores, that can be released by exogenous carbachol. The results are consistent with the presence of a functional Na+-Ca2+ exchanger in the surface membrane. The lack of effect of low-Na+ solutions on contractures evoked by membrane depolarization is consistent with this conclusion. The reduction of the nerve-mediated contraction by low-Na+ solution might result from blockade of the nerve action potential.
确定钠钙交换在调节离体逼尿肌平滑肌收缩性中的作用。
使用离体豚鼠逼尿肌条记录以下方式产生的等长张力：(a) 电场刺激以引发神经介导的反应；(b) 添加卡巴胆碱或用高钾溶液灌流。细胞外和细胞内区室之间的[Na⁺]梯度通过以下方式改变：(i) 逐步将灌流液[Na⁺]从140.2 mmol/L降至10.2 mmol/L；(ii) 添加强心苷毒毛花苷（200 μmol）。结果降低细胞外[Na⁺]可逆地降低神经介导的收缩幅度，但增加静息张力和卡巴胆碱诱导的挛缩幅度。对收缩减弱产生半数最大效应所需的平均（标准差）[Na⁺]为85.9（6.2）mmol/L，对挛缩产生半数最大效应所需的平均（标准差）[Na⁺]为59.1（14.3）mmol/L，二者显著不同。神经介导的收缩和卡巴胆碱挛缩的变化时间常数也显著不同，分别为147（5）秒和1207（386）秒。这些差异表明在低钠溶液中，不同机制影响神经介导的收缩和挛缩。暴露于强心苷毒毛花苷对卡巴胆碱挛缩产生与低钠溶液类似的作用。低钠溶液对高细胞外[K⁺]诱导的挛缩无显著影响。结论降低跨膜[Na⁺]差异会增加细胞内[Ca²⁺]。这种增加主要被细胞内储存所容纳，外源性卡巴胆碱可使其释放。结果与表面膜中存在功能性钠钙交换体一致。低钠溶液对膜去极化诱发的挛缩无影响与该结论相符。低钠溶液使神经介导的收缩减弱可能是由于神经动作电位受阻。
