Cell volume in vascular smooth muscle is regulated by bumetamide
-sensitive ion transport.
Orlov, Sergei N., Johanne Tremblay, and Pavel Hamet.
Centre de Recherche H[circumflex]otel-Dieu de Montr[acute]eal,
Universit[acute]e de Montr[acute]eal, Montr[acute]eal, Qu[acute]ebec,
Canada, Laboratory of Biomembranes, Faculty of Biology, University of
Moscow, Moscow, Russia
APStracts 3:0006C, 1996.
Vascular smooth muscle cells (VSMC) exhibit shrinkage-induced,
bumetanide-inhibited 86Rb influx and ethylisopropylamiloride (EIPA)
-inhibited 22Na influx. In this study, we examined the role of these
transport pathways in volume adjustment of VSMC after isosmotic and
hyperosmotic shrinkage. Cell volume was assessed by measurement of
[14C]-urea distribution. An initial 18-22% cell volume decrease in
isosmotically-shrunken VSMC was followed by a regulatory volume
increase (RVI). RVI was completely abolished by bumetanide but not by
EIPA. No RVI was noted in hyperosmotically-shrunken VSMC. The initial
rate of bumetanide-inhibited 86Rb influx was 2- to 3-fold higher in
isosmotically-shrunken VSMC than with hyperosmotic shrinkage.
Hyperosmotic shrinkage of VSMC was accompanied by a 3- to 4-fold
increase in the rate of bumetanide-inhibited 86Rb efflux, whereas
isosmotic shrinkage augmented this component by only 20-30%. In
contrast to bumetanide-inhibited 86Rb influx, isosmotic shrinkage
slightly increased the rate of EIPA-sensitive 22Na influx.
Hyperosmotic shrinkage led to transient activation of EIPA-inhibited
22Na influx that was completely abolished in 15 min. Activation of
cAMP signalling with isoproterenol arborized VSMC and decreased their
volume by 15%. A similar volume decrease was seen in VSMC treated
with the microfilament-disrupting compound, cytochalasin B. The
isoproterenol-induced cell volume decrease was prolonged by the
addition of bumetanide. Unlike isoproterenol, agents that raise
intracellular Ca2+ (A 23187 and angiotensin II) did not modify VSMC
volume. Thus, our data demonstrate involvement of cAMP signalling in
the regulation of VSMC volume and a key role of bumetanide-inhibited
ion transport in the RVI following isosmotically-induced shrinkage.
Received 3 May 1995; accepted in final form 29 November 1995.
APS Manuscript Number C243-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96