Modulation of cell membrane potential in cultured vascular
endothelium.
Vaca, L Licea A & Possani Ld.
Department of Molecular Physiology and Biophysics, Baylor College
of Medicine, Houston, Texas 77030 and Departamento de Bioenergetica y
Biomembranas, Instituto de Fisiologia Celular, Uiversidad Nacional
Autonoma de Mexico, Apartado Postal 70-600, Mexico D. F. 04510,
Department of Molecular Recognition and Structural Biology, Instituto
de Biotecnologia, Universidad Nacional Autonoma de M[acute]exico.
Apartado Postal 510-3,, Cuernavaca, Morelos 62271, M[acute]exico
APStracts 2:0357C, 1995.
The present study explores the role of different ionic conductances in
the regulation of membrane potential under resting conditions and
after bradykinin or thapsigargin stimulation of cultured bovine
aortic endothelial cells (BAEC). Under resting conditions the cell
membrane potential observed was -62 5 mV. The main conductance under
these conditions is an inwardly rectifying potassium channel (IRK).
Application of 50 nM bradykinin (Bk) induced a transient
hyperpolarization to -87 4 mV followed by a sustained depolarization
to -35 5 mV. The transient hyperpolarization was eliminated by 1
[mu]M noxiustoxin (NTX), a blocker of calcium-activated potassium
channels (KCa). The sustained depolarization induced by Bk was
prevented by incubating the cells with the calcium channel blocker
lanthanum (La3+). Thapsigargin (TG) evoked a similar response in
membrane potential with the exception that the onset of the
hyperpolarization was slower compared to Bk. The results presented
here indicate that the cell resting potential is maintained at -62 2
mV by the IRK. Bk or TG stimulation induces a transient
hyperpolarization of approximately -20 mV produced by activation of a
KCa channel. This hyperpolarization is followed by a sustained
depolarization produced by activation of a calcium selective channel
sensitive to La3+.
Received 18 August 1995; accepted in final form 20 September
1995.
APS Manuscript Number C514-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95