Seiss-Geuder M, Mehrke G, Daut J
Physiologisches Institut, Technischen Universität München, Munich, Germany.
J Cardiovasc Pharmacol. 1992;20 Suppl 12:S97-100. doi: 10.1097/00005344-199204002-00028.
Electrophysiological experiments on cultured monolayers of guinea pig coronary endothelial cells were performed to substantiate the hypothesis that variation of the endothelial membrane potential may be a functionally important mechanism that contributes to the regulation of coronary blood flow. The endothelial cells were loaded with sodium by superfusion with K(+)-free solution at 37 degrees C for 5-30 min. Readmission of external K+ produced a transient hyperpolarization of up to 85 mV, which was due to stimulation of the electrogenic pump current. In most but not all of the monolayers, superfusion with 2 microM adenosine elicited a transient or a sustained hyperpolarization. The transient hyperpolarization had an amplitude of 15 +/- 6 mV. The sustained hyperpolarization had an amplitude of 11 +/- 3 mV. Our results are in line with the hypothesis that the hyperpolarization of the endothelium induced by release of adenosine into the perivascular space of the capillaries may be conducted electronically to the terminal arterioles and may cause vasodilation via current flow through myoendothelial gap junctions.
对豚鼠冠状动脉内皮细胞培养单层进行了电生理实验，以证实以下假说：内皮细胞膜电位的变化可能是一种功能上重要的机制，有助于调节冠状动脉血流量。通过在37℃下用无钾溶液灌流5 - 30分钟，使内皮细胞加载钠。重新引入外部钾离子会产生高达85 mV的瞬时超极化，这是由于电生泵电流受到刺激所致。在大多数但并非所有的单层细胞中，用2 microM腺苷灌流会引发瞬时或持续的超极化。瞬时超极化的幅度为15±6 mV。持续超极化的幅度为11±3 mV。我们的结果与以下假说一致：腺苷释放到毛细血管的血管周围间隙中所诱导的内皮超极化可能通过电传导至终末小动脉，并可能通过流经肌内皮间隙连接的电流引起血管舒张。
