WANG Ru-xing, LI Xiao-rong, YANG Zhen-yu, LI Ku-lin, ZHENG Jie, ZHANG Chang-ying, GUO Su-xia, SUN Li-ping, LU Tong
Department of Cardiology, Affiliated People's Hospital of Nanjing Medical University, Wuxi Municipal People's Hospital, Wuxi 214023, China.
Zhonghua Yi Xue Za Zhi. 2010 Sep 28;90(36):2575-8.
to investigate the regulation in vascular tension of diabetic coronary artery by large conductance Ca(2+)-activated K(+) channel (BK channel) and to elucidate the mechanisms of coronary dysfunctions due to diabetes.
regulation of vascular tension in normal coronary artery was evaluated by videomicroscopy system. Streptozotocin-induced rat diabetic animal model was established successfully by intraperitoneal injection. Coronary smooth muscle cells were isolated by enzyme digestion. The BK currents in control and diabetic groups were recorded by patch clamp technique in whole cell configuration. Changes of vascular tension in normal and diabetic coronary arteries were assayed by multi-wire myograph system.
more than 50% was contracted in inner diameters of coronary arteries when 100 nmol/L IBTX, a specific BK channel blocker, was applied. In comparison with normal group, the BK current densities in diabetic group significantly decreased when test potentials were more than 60 mV (P < 0.05). The BK current densities at 150 mV in normal group and diabetic group were (275 ± 40) pA/pF and (70 ± 10) pA/pF respectively. When 100 mmol/L KCl was washed out, vascular tensions of normal and diabetic coronary artery were (398 ± 38) mg and (390 ± 35) mg respectively (P > 0.05); however, when 100 nmol/L IBTX was added, the vascular tensions of normal and diabetic coronary artery were (395 ± 40) mg and (50 ± 7) mg (P < 0.05).
BK channels play an important role in the regulation of coronary vascular tension, whereas BK channels in diabetic coronary artery are dysfunction, BK currents decrease and vascular tensions increase.
研究大电导钙激活钾通道(BK通道)对糖尿病冠状动脉血管张力的调节作用,以阐明糖尿病所致冠状动脉功能障碍的机制。
采用视频显微镜系统评估正常冠状动脉的血管张力调节。通过腹腔注射成功建立链脲佐菌素诱导的大鼠糖尿病动物模型。采用酶消化法分离冠状动脉平滑肌细胞。采用全细胞膜片钳技术记录对照组和糖尿病组的BK电流。采用多线肌张力测定系统检测正常和糖尿病冠状动脉血管张力的变化。
应用特异性BK通道阻滞剂100 nmol/L Iberiotoxin(IBTX)时,冠状动脉内径收缩超过50%。与正常组相比,当测试电位大于60 mV时,糖尿病组的BK电流密度显著降低(P<0.05)。正常组和糖尿病组在150 mV时的BK电流密度分别为(275±40)pA/pF和(70±10)pA/pF。当洗脱100 mmol/L KCl时,正常和糖尿病冠状动脉的血管张力分别为(398±38)mg和(390±35)mg(P>0.05);然而,当加入100 nmol/L IBTX时,正常和糖尿病冠状动脉的血管张力分别为(395±40)mg和(50±7)mg(P<0.05)。
BK通道在冠状动脉血管张力调节中起重要作用,而糖尿病冠状动脉中的BK通道功能障碍,BK电流降低,血管张力增加。