Impairment of Ca(2+) mobilization in circular muscle cells of the inflamed colon.
Impairment of Ca(2+) mobilization in circular muscle cells of the inflamed colon.
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DOI：
10.1152/ajpgi.2000.278.2.g234
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发表时间：
2000-02
期刊：
影响因子：
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通讯作者：
Xuan-Zheng Shi;Sushil K. Sarna
中科院分区：
文献类型：
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作者：
Xuan-Zheng Shi;Sushil K. Sarna
本研究探讨炎症是否调节犬结肠环形肌细胞Ca（2+）的动员。发炎结肠单细胞的收缩反应在ACh、KCl和BAY K8644的作用下被显著抑制。甲氧维拉帕米和细胞外Ca（2+）浓度的降低剂量依赖性地阻断了正常细胞和炎症细胞的反应。炎症细胞中响应ACh和KCl的细胞内Ca（2+）浓度的增加明显减少。然而，ryanodine-和肌醇1,4,5 -三磷酸（IP(3)）敏感储存的Ca（2+）外排以及响应于ryanodine和IP(3)的细胞长度减少不受影响。肝素在两种情况下均可显著阻断钙（2+）的外排和对乙酰胆碱的收缩。乙酰胆碱刺激的IP积累(3)和[(3)H]ryanodine与其受体的结合不因炎症而改变。钌红部分抑制正常和炎症状态下对乙酰胆碱的反应。我们得出结论，犬结肠环形肌细胞利用钙（2+）通过l型通道流入，以及钙（2+）从ryanodine和IP(3)敏感储存中释放来收缩。炎症损害钙（2+）通过l型通道流入，但可能不影响细胞内钙（2+）的释放。Ca（2+）内流的损害可能导致炎症状态下圆形肌肉收缩力的抑制。
This study investigated whether inflammation modulates the mobilization of Ca(2+) in canine colonic circular muscle cells. The contractile response of single cells from the inflamed colon was significantly suppressed in response to ACh, KCl, and BAY K8644. Methoxyverapamil and reduction in extracellular Ca(2+) concentration dose-dependently blocked the response in both normal and inflamed cells. The increase in intracellular Ca(2+) concentration in response to ACh and KCl was significantly reduced in the inflamed cells. However, Ca(2+) efflux from the ryanodine- and inositol 1,4, 5-trisphosphate (IP(3))-sensitive stores, as well as the decrease of cell length in response to ryanodine and IP(3), were not affected. Heparin significantly blocked Ca(2+) efflux and contraction in response to ACh in both conditions. ACh-stimulated accumulation of IP(3) and the binding of [(3)H]ryanodine to its receptors were not altered by inflammation. Ruthenium red partially inhibited the response to ACh in normal and inflamed states. We conclude that the canine colonic circular muscle cells utilize Ca(2+) influx through L-type channels as well as Ca(2+) release from the ryanodine- and IP(3)-sensitive stores to contract. Inflammation impairs Ca(2+) influx through L-type channels, but it may not affect intracellular Ca(2+) release. The impairment of Ca(2+) influx may contribute to the suppression of circular muscle contractility in the inflamed state.