Functional role of ATP-sensitive K^+ channel in vascular endothelial cells

据报道，在Kir6.2基因缺陷或SUR2基因缺陷的小鼠中观察到了印迹金属型心绞痛。为了确定血管痉挛心绞痛小鼠血管痉挛心绞痛的发生是否与血管内皮细胞ATP敏感性钾通道功能障碍有关，我们采用膜片钳技术和实时荧光定量聚合酶链式反应技术，研究了血管痉挛心绞痛小鼠对钾通道开放剂的电生理反应和基因表达。K~+通道开放剂对野生型小鼠肺组织分离的血管内皮细胞和培养的小鼠肺内皮细胞(UV细胞)膜电位无明显影响。在这些内皮细胞中几乎没有检测到与KATP通道相关的离子通道基因。而在小鼠膀胱组织中，RT-PCR检测到Kir6.1和SUR2B基因的表达。K~+通道开放剂吡那地尔在野生型和Kir6.2缺陷小鼠的内脏平滑肌细胞上诱发KATP电流，但对Kir6.1缺陷小鼠的KATP电流无明显影响。这些结果提示，血管内皮细胞上的KATP通道不太可能在小鼠血管痉挛心绞痛的诱导中起重要作用。

It has been reported that Prinzmetal-type angina pectoris is observed in Kir6.2-deficient or SUR2-deficient mice. In order to determine whether dysfunction of ATP-sensitive K^+ (KATP) channels in endothelial cells is involved in the development of vasospastic angina in Kir6.2-deficient or SUR2-deficient mice, we evaluated elecrophysiological responses to K^+ channel openers by using patch clamp techniques and gene expression by using real time PCR in endothelial cells. K^+ channel openers failed to affect the membrane potentials in vascular endothelial cells isolated from pulmonary tissues of wild type mouse and cultured mouse endothelial cells (UV cells). Ion channel genes related to KATP channels were hardly detected in these endothelial cells. In contrast, in mouse urinary bladder mRNA of Kir6.1 and SUR2B could be detected by RT-PCR. The K^+ channel opener pinacidil induced KATP current in visceral smooth muscle cells of wild type and Kir6.2-deficient mice, but not those of Kir6.1-deficient mice. These results suggest that KATP channel in vascular endothelial cells is unlikely to play an important role in the induction of vasospastic angina in mouse.