Hyperglycemia alters cytoplasmic ca2+ responses to capacitative
ca2+ influx in rat aortic smooth muscle cells.
Rivera, Angel A., C. Roger White, Lisa L. Guest, Terry S. Elton, and
Richard B. Marchase.
Department of Cell Biology and Hypertension Program, Division of
Cardiovascular Diseases Department of Medicine, The University of
Alabama at Birmingham, Birmingham, AL 35294-0005
APStracts 2:0222C, 1995.
Concentrations of free cytoplasmic Ca2+ in rat aortic smooth muscle
(RASM) cells were monitored using the ratiometric Ca2+ indicator
Fura-2AM. In RASM cells cultured in 5 mM Glc incubation with
angiotensin II, ATP, or thapsigargin (a selective inhibitor of the
sarcoplasmic reticulum (SR) Ca2+ATPase) depleted SR Ca2+ stores and
initiated a capacitative Ca2+ influx through the plasma membrane.
This influx was resistant to verapamil, a selective inhibitor of L
-type voltage-gated Ca2+ channels, but was sensitive to SKF 96365, an
inhibitor of the receptor-operated Ca2+ entry pathway. RASM cells
cultured in 25 mM Glc exhibited a significant decrease in cytoplasmic
Ca2+ responses to agonist-induced Ca2+ release from SR stores and to
subsequent capacitative Ca2+ entry. In addition, the cytoplasmic
response to thapsigargin-induced release of Ca2+ from the SR in
hyperglycemic cells peaked more sharply than in control cells and
returned to baseline more rapidly. The effects of hyperglycemia were
not overcome by myo-inositol supplementation.
Received 23 February 1995; accepted in final form 26 May 1995.
APS Manuscript Number C98-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 June 1995.