CONTRIBUTIONS OF K- TO THE MEMBRANE-POTENTIAL OF INTACT HAMSTER VASCULAR ENDOTHELIAL-CELLS(, NA+, AND CL)

The transmembrane potential (V(m)) of vascular endothelial cells (EC) is an important property that may be involved in intra- and intercellu lar signal transduction for various vascular functions. In this study, V(m) of intact aortic and vena caval EC from hamsters were measured u sing conventional microelectrodes. Vascular strips with the luminal su rface upwards were suffused in a tissue chamber with Krebs solution in physiological conditions. The resting V(m) of aortic and vena caval E C was found to be -40 +/- 1 mV (n = 55) and -43 +/- 1 mV (n = 15), res pectively. The V. recordings were confirmed to have originated from EC by scanning and transmission electron microscopy combined with the co mparison of electrical recordings between normal and endothelium-denud ed aortic strips. The input resistance varied from 10-240 MOMEGA, whic h implied the presence of electrical coupling between vascular EC. Ele vating the K+ level in the suffusate from 4.7 mM to 50 and 100 mM depo larized aortic EC by 19% and 29% and vena caval EC by 18% and 29%, res pectively. These low percentages indicated a relatively small contribu tion of [K+] to the resting V(m) of vascular EC. A positive correlatio n (r > 0.69) between the resting V(m) and the magnitude of depolarizat ion by the high [K+]. may be related to the involvement of voltage-dep endent K+ channels. The hyperpolarization caused by lowering both [Na]o and [Cl-]o suggested the disengagement of some electrogenic transpo rt systems in the membrane, such as a Na+-K+-Cl- cotransporter. The tr ansference number (t(ion)), as an index of membrane conductance for sp ecific 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 V(m). Our study documented some basic electrophysiolo gy of the vascular EC when both structural and functional properties o f the cell were maintained, thus furthering the understanding of the e ssential role of endothelial cells in mediating vascular functions. (C ) 1993 Wiley-Liss, Inc.