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目的探讨T型钙通道在实验性糖尿病肾病中的作用。方法采用单侧肾切除（UNx）的糖尿病大鼠模型，分别每日灌胃给予T型钙通道阻滞剂米贝地尔（Mib）、L型钙通道阻滞剂氨氯地平（Aml）、血管紧张素转换酶抑制剂西拉普利（Cil）、及Mib与Cil合用（M＋C），共4周，并使各药物处理组血压相近（每组n＝6~8）。结果Mib、Cil和M＋C治疗组较未治疗的糖尿病（DM）组尿白蛋白量明显减少（Mib：7．69±1．87，Cil：5.53±1．45，M＋C：3.87±0．88比DM：17．67±4．90，单位为μg／24h；P＜0．05），增高的Ccr下降。病理学检查显示Mib、Cil与M＋C组肾小球Ⅳ型胶原、层粘连蛋白显著少于DM。Aml对尿白蛋白量、肾小球基质和Ⅳ型胶原量无明显改善作用，但也可减少尿蛋白、Ccr和肾小球层粘连蛋白含量。M＋C治疗组的肾小球基质和Ⅳ型胶原量在各糖尿病大鼠中最低（均P＜0．05）。结论阻断T型钙通道可减轻糖尿病大鼠的蛋白尿和肾小球基质沉积，与ACE抑制剂合用有额外的保护效应，提示T型钙通道在糖尿病肾病中的作用不同于血管紧张素和L型钙通道，其机制有待进一步研究。
Objective To investigate the role of T-type calcium channel in experimental diabetic nephropathy. Methods Unilateral nephrectomized (UNx) diabetic rat models were given intragastric administration of T-type calcium channel blocker Mib, L-type calcium channel blocker Amlodipine, The angiotensin-converting enzyme inhibitor cil, and Mib combined with Cil (M + C) for 4 weeks resulted in similar blood pressure (n = 6 to 8 for each group). Results Compared with untreated diabetic group, the levels of urinary albumin in Mib, Cil and M + C groups were significantly decreased (Mib: 7.69 ± 1.87, Cil: 5.53 ± 1.45, M + C: 3.87 ± 0.88 DM: 17.67 ± 4.90 in μg / 24h; P <0.05), increased Ccr decreased. Pathological examination showed that glomerular type IV collagen and laminin were significantly less than DM in Mib, Cil and M + C groups. Aml on urinary albumin, glomerular matrix and collagen type Ⅳ no significant improvement, but also reduce urinary protein, Ccr and glomerular laminin content. The amount of glomerular matrix and type IV collagen in M + C treatment group was the lowest in all the diabetic rats (all P <0.05). Conclusion Blocking T-type calcium channels can reduce the proteinuria and glomerular matrix deposition in diabetic rats, and there is an additional protective effect in combination with ACE inhibitors, suggesting that T-type calcium channels play a different role in diabetic nephropathy than angiotensin L-type calcium channel, the mechanism remains to be further studied.