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

有报道称，在kir6.2缺乏或sur2缺乏的小鼠中观察到prinzmetal型心绞痛。为了确定内皮细胞中atp敏感的K^+ (KATP)通道功能障碍是否参与kir6.2缺陷或sur2缺陷小鼠血管痉挛性心绞痛的发展，我们使用膜片钳技术和内皮细胞中实时PCR的基因表达来评估K^+通道打开剂的电生理反应。K^+通道打开剂对野生型小鼠和培养小鼠内皮细胞（UV细胞）肺组织血管内皮细胞的膜电位没有影响。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。RT-PCR可检测小鼠膀胱中Kir6.1和SUR2B mRNA的表达。K^+通道开启剂pinacidil诱导野生型和kir6.2缺陷小鼠内脏平滑肌细胞的KATP电流，而kir6.1缺陷小鼠内脏平滑肌细胞无KATP电流。这些结果提示，血管内皮细胞中的KATP通道不太可能在小鼠血管痉挛性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.