No evidence for a role of reverse na+/ca2+ exchange in insulin
release from mouse pancreatic islets.
Garcia-Barrado, Maria-Jose, Patrick Gilon, Yoshihiko Sato, Myriam
Nenquin, and Jean-Claude Henquin.
Unit[acute]e d'Endocrinologie et M[acute]etabolisme, University of
Louvain School of Medicine, UCL 55.30, B-1200 Brussels, Belgium
APStracts 3:0088E, 1996.
We studied whether reverse Na+/Ca2+ exchange can increase cytoplasmic
Ca2+ ([Ca2+]i) in mouse islets and contribute to insulin release. The
exchange was stimulated by replacing Na+ with choline, sucrose or
lithium in a medium containing 15 mM glucose. Na+ omission increased
electrical activity in B-cells, [Ca2+]i and insulin release. When
voltage-dependent Ca2+ channels were blocked by nimodipine or closed
by holding the membrane polarized with diazoxide, Na+ omission caused
a slight hyperpolarization, a small rise in [Ca2+]i and a marginal
increase in insulin release (the latter only with choline). This
small rise in [Ca2+]i was dependent on extracellular Ca2+, but was
hardly augmented when intracellular Na+ was raised with alanine. When
B-cells were depolarized by 30 mM K+, Na+ omission did not affect the
membrane potential, but increased [Ca2+]i and insulin release. If
Ca2+ channels were blocked by nimodipine, only marginal increases in
Ca2+ and insulin release persisted, which were not different from
those observed when the cells were not depolarized. This indicates
that Ca2+ influx through voltage-dependent Ca2+ channels rather than
via reverse Na+/Ca2+ exchange underlies the rise in [Ca2+]i and in
insulin release produced by Na+ removal. No decisive support for Ca2+
influx by reverse Na+/Ca2+ exchange could be found.
Received 12 February 1996; accepted in final form 8 April 1996.
APS Manuscript Number E81-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96