Bény J L, Zhu P, Haefliger I O
Department of Zoology and Animal Biology, Sciences III, Geneva University, Switzerland.
J Vasc Res. 1997 Sep-Oct;34(5):344-50. doi: 10.1159/000159243.
In porcine coronary artery, bradykinin-induced endothelium-dependent vasodilatations are associated with simultaneous endothelium as well as endothelium-dependent smooth muscle cell (SMC) hyperpolarizations. In contrast, in porcine ciliary artery bradykinin evokes endothelium-dependent relaxations, but no change in SMC membrane potential. This study addresses the question of whether the lack of bradykinin-induced SMC hyperpolarization is also associated with an absence of endothelial hyperpolarization in porcine ciliary artery. With a microelectrode to impale cells in arterial strips, a 12-mV transient bradykinin-induced hyperpolarization was measured in endothelial cells. Bradykinin evoked no SMC hyperpolarization deep in the media. Only occasionally, a slight 4-mV hyperpolarization could be recorded in some SMC next to the endothelium. The endothelial intracellular injection (through the recording electrode) of the fluorescent tracers, lucifer yellow or ethidium bromide, showed the existence of a heterocellular dye coupling between endothelial cells and SMC. These observations in porcine ciliary artery demonstrate that the lack of bradykinin-induced endothelium-dependent SMC hyperpolarization is not due to an absence of endothelial cell hyperpolarization, but most likely to an insufficient electrotonic propagation space constant from endothelial cells to SMC, despite the presence of a dye coupling between these cells.
在猪冠状动脉中，缓激肽诱导的内皮依赖性血管舒张与内皮同时发生的超极化以及内皮依赖性平滑肌细胞（SMC）超极化有关。相比之下，在猪睫状动脉中，缓激肽可引起内皮依赖性舒张，但SMC膜电位无变化。本研究探讨了猪睫状动脉中缓激肽诱导的SMC超极化缺失是否也与内皮超极化缺失相关的问题。用微电极刺入动脉条中的细胞，在内皮细胞中测量到缓激肽诱导的12 mV瞬时超极化。缓激肽在中膜深层未引起SMC超极化。仅偶尔能在靠近内皮的一些SMC中记录到轻微的4 mV超极化。通过记录电极向内皮细胞内注射荧光示踪剂荧光素黄或溴化乙锭，显示内皮细胞与SMC之间存在异细胞染料偶联。在猪睫状动脉中的这些观察结果表明，缓激肽诱导的内皮依赖性SMC超极化缺失并非由于内皮细胞超极化缺失，而是很可能由于从内皮细胞到SMC的电紧张传播空间常数不足，尽管这些细胞之间存在染料偶联。
