Contributions of K+, Na+, and Cl- to the membrane potential of intact hamster vascular endothelial cells.

The transmembrane potential (Vm) of vascular endothelial cells (EC) is an important property that may be involved in intra- and intercellular signal transduction for various vascular functions. In this study, Vm of intact aortic and vena caval EC from hamsters were measured using conventional microelectrodes. Vascular strips with the luminal surface upwards were suffused in a tissue chamber with Krebs solution in physiological conditions. The resting Vm of aortic and vena caval EC was found to be -40 +/- 1 mV (n = 55) and -43 +/- 1 mV (n = 15), respectively. The Vm recordings were confirmed to have originated from EC by scanning and transmission electron microscopy combined with the comparison of electrical recordings between normal and endothelium-denuded aortic strips. The input resistance varied from 10-240 M omega, which implied the presence of electrical coupling between vascular EC. Elevating the K+ level in the suffusate from 4.7 mM to 50 and 100 mM depolarized aortic EC by 19% and 29% and vena caval EC by 18% and 29%, respectively. These low percentages indicated a relatively small contribution of [K+] to the resting Vm of vascular EC. A positive correlation (r > 0.69) between the resting Vm and the magnitude of depolarization by the high [K+]o may be related to the involvement of voltage-dependent K+ channels. The hyperpolarization caused by lowering both [Na+]o and [Cl-]o suggested the disengagement of some electrogenic transport systems in the membrane, such as a Na(+)-K(+)-Cl- cotransporter. The transference number (t(ion)), as an index of membrane conductance for specific ions, was calculated for K+ (15-20%), Na+ (16%), and Cl- (9-15%), demonstrating that both Na+ and Cl- as well as K+ contribute to the overall resting Vm. Our study documented some basic electrophysiology of the vascular EC when both structural and functional properties of the cell were maintained, thus furthering the understanding of the essential role of endothelial cells in mediating vascular functions.