Wang R, Liu Y, Sauvé R, Anand-Srivastava M B
Department of Physiology, Université de Montréal, Québec, Canada.
Mol Cell Biochem. 1998 Jun;183(1-2):79-85. doi: 10.1023/a:1006813223216.
Hyperglycemia and/or hyperosmolality may disturb calcium homeostasis in vascular smooth muscle cells (SMCs), leading to altered vascular contractility in diabetes. To test this hypothesis, the KCl-induced increases in [Ca2+]i in primarily cultured vascular SMCs exposed to different concentrations of glucose were examined. With glucose concentration in solutions kept at 5.5 mM, KCl induced a fast increase in [Ca2+]i which then slowly declined (type 1 response) in 83% of SMCs from non-diabetic rats. In 9% of non-diabetic SMCs KCl induced a slow increase in [Ca2+]i (type 2 response). Interestingly, under the same culture conditions KCl induced type 1 and type 2 responses in 47 and 35% of SMCs from diabetic rats. When SMCs from non-diabetic or diabetic rats were cultured in 36 mM glucose, KCl induced a fast increase in [Ca2+]i which, however, maintained at a high level (type 3 response). The sustained level of [Ca2+]i in the presence of KCl was significantly higher in cells cultured with 36 mM glucose than that in non-diabetic cells cultured with 5.5 mM glucose. Furthermore, the hyperglycemia-induced alterations in calcium mobilization were similarly observed in cells cultured in high concentration of mannitol (30.5 mM) or L-glucose, indicating that hyperosmolality was mainly responsible for the abnormal calcium mobilization in diabetic SMCs.
高血糖和/或高渗状态可能会扰乱血管平滑肌细胞（SMC）中的钙稳态，导致糖尿病患者血管收缩性改变。为了验证这一假设，研究人员检测了在不同葡萄糖浓度下，氯化钾诱导的原代培养血管平滑肌细胞内钙离子浓度（[Ca2+]i）的增加情况。当溶液中的葡萄糖浓度保持在5.5 mM时，氯化钾能诱导非糖尿病大鼠83%的平滑肌细胞内[Ca2+]i快速升高，随后缓慢下降（1型反应）。在9%的非糖尿病平滑肌细胞中，氯化钾诱导[Ca2+]i缓慢升高（2型反应）。有趣的是，在相同培养条件下，氯化钾能诱导糖尿病大鼠47%的平滑肌细胞产生1型反应，35%的平滑肌细胞产生2型反应。当非糖尿病或糖尿病大鼠的平滑肌细胞在36 mM葡萄糖中培养时，氯化钾诱导[Ca2+]i快速升高，但随后维持在较高水平（3型反应）。在36 mM葡萄糖培养的细胞中，氯化钾存在时[Ca2+]i的持续水平显著高于在5.5 mM葡萄糖培养的非糖尿病细胞。此外，在高浓度甘露醇（30.5 mM）或L-葡萄糖培养的细胞中，也观察到了高血糖诱导的钙动员改变，这表明高渗状态是糖尿病平滑肌细胞钙动员异常的主要原因。
