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Documenti di Professioni
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a comparative
view
M. E. CHAMBERLIN
AND K. STRANGE
Department
of Zoological and Biomedical Sciences and College of Osteopathic Medicine,
Ohio University,
Athens 45701; and Department
of Physiology and Biophysics,
Wright State University
School of Medicine, Dayton, Ohio 45435
CHAMBERLIN, M. E., AND K. STRANGE. Anisosmotic ceZZuohne regulation: a comparative view. Am. J. Physiol. 257 (Cell Physiol. 26): Cl59-Cl73,
1989.-A
variety of organisms and cell types spanning the five taxonomic
kingdoms are exposed, either naturally or through experimental
means, to
osmotic stresses. A common physiological
response to these challenges is
maintenance
of cell volume through changes in the concentration
of intracellular inorganic
and organic solutes, collectively termed osmolytes. Research on the mechanisms by which the concentration
of these solutes is
regulated has proceeded along several experimental
lines. Extensive studies
on osmotically activated ion transport pathways have been carried out in
vertebrate cells and tissues. Much of our knowledge on organic osmolytes
has come from investigations
on invertebrates,
bacteria, and protists. The
relative simplicity of bacterial genetics has provided a powerful and elegant
tool to explore the modifications
of gene expression during volume regulation. An implication
of this diverse experimental
approach is that phylogenetically divergent organisms employ uniquely adapted mechanisms
of
cell volume regulation.
Given the probability
that changes in extracellular
osmolality were physiological
stresses faced by the earliest organisms, it is
more likely that cell volume regulation
proceeds by highly conserved
physiological
processes. We review volume regulation
from a comparative
perspective, drawing examples from all five taxonomic kingdoms. Specifically, we discuss the role of inorganic
and organic solutes in volume
maintenance
and the mechanisms
by which the concentrations
of these
osmolytes are regulated. In addition,
the processes that may transduce
volume perturbations
into regulatory responses, such as stretch activation
of ion channels, intracellular
signaling, and genomic regulation,
are discussed. Throughout
this review we emphasize areas we feel are important
for future research.
osmotic stress; osmolytes;
membrane
OF cell volume is a fundamental physiological process. Under isosmotic conditions cell swelling
tends to occur because of the presence of negatively
charged macromolecules in the cytoplasm. This swelling,
however, is counteracted by active extrusion of solutes,
such as Na+ via the Na+-K+-ATPase. In contrast, exposure to anisosmotic media drives water into or out of the
cell due to alterations in extracellular osmolality. Many
cells studied to date respond to these anisosmotically
induced volume changes by modulating membrane transport and/or metabolic pathways that alter the concentration of intracellular solutes. The processesresponsible
for returning cell volume toward its original value after
osmotic swelling or shrinkage are termed regulatory volMAINTENANCE
0363-6143/89
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transport;
cellular
metabolism
Physiological
Society
Cl59
Cl60
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REVIEW
Mechanism
Regulatory
K+-H+ exchangers
Parallel Cl--HCO?
exchangers
K+ channels
and K+-H+
K+ or KC1 loss
Unidentified
Ca2+-dependent
pathways
Parallel
Na-H
exchangers
and Cl--HCOc
NaCl cotransporters
Na+-K+-2Clcotransporters
K+ pumps
Cl- pumps
red blood
cells
Bacteria
Amphibian
urinary
bladder
Amphibian
gallbladder
Lymphocytes
Ehrlich
ascites cells
Mammalian
renal tubules
Lymphocytes
Ehrlich
ascites cells
Teleost red blood cells
Avian red blood cells
Mammalian
red blood cells
Annelid
coelomocytes
Molluscan
red blood cells
Crustacean
nerves and
muscle fibers
Horseshoe
crab myocardium
Canine red blood cells
KC1 cotransporters
Unidentified
pathways
Type
decrease
Bacteria
Amphibian
Cl- channels
OSMOLYTES
Inorganic ions. Inorganic ion transport has been implicated in cell volume regulati .on in a wide of variety
organisms (Table 1). The extent of information available
on volume regulatory ion transport pathways in animals,
plants, moneran .S fungi, and protists is, however, extremely variable Ion transport pathways activated bY
changes in environmental osmolality have been examined in some detail in protists (algae) and monerans
(bacteria and cyanobacteria). Species in these two kingdoms that are surrounded by rigid cell walls maintain a
internal
hydrostatic
pressure
significant
positive
gradient. This so-called turgor pressure is regulated
within narrow physiological limits and is generated by
the accumulation of solutes and water in the cytoplasm.
In organisms with rigid cell walls, external osmolality
has variable effects on cell volume. Exposure to hypertonic stress causes cell shrinkage and loss of turgor
pressure, whereas hypotonicity results in increased turgor pressure but may have little or no effect on cell
volume. The presence of a cell wall will obviously limit
or prevent cell swelling. This dual nature of cell volume
change in walled organ isms makes it difficult to separate
the process of turgor regulation from that of volume
regulation per se. What is clear, however, is that variations in transmembrane hydrostatic and osmotic pressure gradients result in the activation of specific ion
transport pathways that return these parameters to their
original values.
Detailed studies on volume regulatory ion transport
have been conducted in giant algal cells, such as Valonia,
Nitella, and Halicystis. When exposed to hypertonic
stress, these organisms activate K+ or Cl- pumps that
drive net salt and water uptake and that are responsible
for restoration of cell volume and turgor (reviewed in
Ref. 69). The mechanisms responsible for reducing cell
volume and turgor in hypotonically stressed algal cells
have not been studied in any detail.
volume
or Cell
volume
increase
Amphibian
red blood cells
Amphibian
gallbladder
Lymphocytes
Mammalian
renal tubules
Mammalian
red blood cells
Ehrlich
ascites cells
Amphibian
skin
Avian red blood cells
Ehrlich
ascites cells
Cultured
canine kidney
cells
(MDCK)
Bacteria
Algae
Algae
See Refs. 47, 48, 50, 56, 65, 69, 72, 79, 80, 99, 128, 140,
detailed discussions
of these pathways.
143 for
INVITED
Cl61
REVIEW
Sugars
Monosaccharides
(e.g., glucose,
mannose,
fructose)
Disaccharides
trehalose)
(e.g., sucrose,
inositol,
Methylamines
(e.g., betaine,
sarcosine,
glycerophosphorylcholine)
Urea
Cyanobacteria
Diatoms
Fungi
Cyanobacteria
Eubacteria
Algae
Plants
Insects
Crustaceans
Cyanobacteria
Algae
Fungi
Plants
Insects
Crustaceans
Mammalian
renal cells
Mammalian
brain cells
Eubacteria
Plants
Annelids
Mollusks
Crustaceans
Elasmobranch
red blood
Teleost red blood cells
Ehrlich
ascites cells
Cyanobacteria
Eubacteria
Plants
Mollusks
Echinoderms
Holocephalans
Agnathans
Elasmobranchs
Teleosts
Mammalian
renal cells
Elasmobranchs
Amphibians
Mammalian
renal cells
cells
See Refs. 10, 18, 22, 26, 27, 35, 36, 46, 51, 53, 58, 78,81, 98, 101, 102,
106, 118, 128, 129, 137, 151, 156, 159, 160 for detailed discussions
of
intracellular
organic
osmolytes.
Cl62
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REVIEW
INVITED
floridoside
(galactosylglycerol)
is accumulated
within
minutes of the onset of hyperosmotic
stress (reviewed in
Refs. 78, 156). This compound is synthesized
from a
storage compound,
chrysolaminarin.
The synthesis
of
this modified polyol depends on the action of isofloridoside phosphate synthetase,
an enzyme that is normally
stored in an inactive form. During hyperosmotic
stress,
cellular proteases activate the enzyme, and synthesis
of
isofloridoside
ensues. It is thought that calmodulin-dependent processes are involved in activating
the proteases. During hyposmotic
stress, the isofloridoside
is
reincorporated
into chrysolaminarin.
It has been suggested that sorbitol may play a role in
cell volume regulation in renal medullary cells. During
antidiuresis
the osmolality
in this region of the mammalian kidney can reach levels X,200 mosmol/kgH20
(90, 104) with a concomitant
increase in medullary sorbitol levels (68, 158, 159). Regulation of sorbitol levels
has been studied in cultured renal medullary cells. Unlike
algal cells, however, the accumulation
of polyols during
RVI in cultured medullary cells is quite slow, taking 1224 h before sorbitol levels rise (152). The carbon source
for sorbitol synthesis is thought to be exogenous glucose
(12, 118), although synthesis
from glycogen, which is
found in intact renal medulla (loo), has not been examined. Synthesis of sorbitol in cultured cells is dependent,
in part, on the induction
of aldose reductase,
which
converts glucose to sorbitol (l&12,19,152;
see SENSORS
AND TRANSDUCERS). In many cells, however, excess glucose is converted to glycogen. To assure that sorbitol is
synthesized from glucose, there must be low activities of
glucokinase and other enzymes involved in glycogen synthesis. This aspect of glucose metabolism
in cultured
renal cells has not been described. If sorbitol is synthesized from glycogen, glycolysis may be modified to increase the levels of glucose 6-phosphate,
which, in turn,
is converted to glucose and ultimately sorbitol. Funneling
carbons to sorbitol synthesis will be potentiated if there
is increased synthesis
and/or decreased degradation of
glucose 6-phosphate.
This aspect of sorbitol metabolism
has not been examined in renal cells but has been extensively studied in freeze-tolerant
insects that synthesize
sorbitol, a cryoprotectant,
from glycogen. During the
period of sorbitol accumulation in these organisms, there
is increased activity of glycogen phosphorylase
and hexokinase (see Ref. 144). At the same time, the catabolism
of glucose 6-phosphate
is restricted
because phosphofructokinase
is inhibited. This inhibition is due, in part,
to a fall in fructose 2,6-bisphosphate,
an activator
of
phosphofructokinase.
This modulator might be involved
in the regulation of renal glycolysis (85) and therefore
may ultimately
affect sorbitol synthesis
in renal cells.
Another point of control in the synthesis of renal sorbitol
may be the concentration
of urea in the medulla. Rabbit
muscle phosphofructokinase
is sensitive to urea and may
not be protected from ureas inhibitory
effects by trimethylamines (71). During antidiuresis,
medullary levels of
urea are very high. It is tempting to speculate that if
renal phosphofructokinase
is similar to muscle phosphofructokinase,
then the presence of high urea concentrations during antidiuresis
would inhibit phosphofructo-
REVIEW
Cl63
Cl64
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REVIEW
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see
SENSORS
AND
REVIEW
Cl65
TRANSDUCERS).
SENSORS
AND
TRANSDUCERS
The mechanisms
in-
Cl66
INVITED
REVIEW
and Sigurdson (116) have described a new class of channels that is inactivated by membrane stretch. These
stretch-inactivated channels coexist with SA channels in
neurons. It is tempting to speculate that these channels
may indirectly play a role in volume regulation. For
example, cell swelling could activate specific volume regulatory K+ and Cl- channels and concomitantly inactivate resting K+ and Cl- conductances. Such a process
might allow the cell to more effectively control membrane function during volume regulation.
Cytoskeleton. Several investigations have implicated a
role for the cytoskeleton in cellular volume maintenance
(see Refs. 37, 52, 59). The function of the cytoskeleton
is likely to be indirect. One possibility is that cytoskeletal
elements may mediate the movement of cytoplasmic
vesicles containing volume regulatory transport proteins
to and from the plasma membrane. Endo- or exocytosis
of these proteins would then control volume regulatory
solute movements. Studies by Lewis and de Moura (103)
provide indirect support for a role of cytoskeleton-mediated vesicle translocation in anisosmotic volume regulation. These investigators demonstrated that exposure
of the rabbit urinary bladder to dilute salines caused a
dramatic increase in apical membrane area as measured
by changes in membrane capacitance. Reexposure of
bladders to isosmotic saline resulted in a return of apical
membrane area to control values. These area changes
appeared to be dependent on an intact microfilament
network, since they were blocked by cytochalasin B.
Whether these cells actually regulate their volume and
whether the observed changes in apical membrane area
are associated with RVD has not been shown.
An interesting possibility is that the cytoskeleton could
act as a sensor of volume-induced changes in membrane
tension and/or stretch. Sachs and co-workers (67, 135)
have attempted to elucidate the factors that determine
the stretch sensitivity of SA channels. These investigators postulated that the sensitivity of a SA channel is
increased when the force from a large membrane area is
gathered to a channel via attachment to submembrane
cytoskeletal elements. Guharay and Sachs (67) provided
experimental evidence supporting this idea by demonstrating that cytochalasins dramatically alter the tension
sensitivity of chick skeletal muscle SA channels.
Volume-induced membrane structural changes. Changes
in the volume of a cell should directly alter the structure
of the plasma membrane by changing the distribution
and packing of membrane lipids and proteins. Such
structural changes could, in theory, directly alter membrane transport pathways and/or signaling mechanisms
involved in volume regulation. Parker and co-workers
(reviewed in Ref. 125) have shown that volume perturbations alter the accessibility of reactive groups on dog
red blood cell membranes to glutaraldehyde or sulfhydryl
reagents. For example, exposure of shrunken cells to Nphenylmaleimide locks the volume regulatory Na+-H+
exchanger in the on mode so that the activity of the
transporter becomes independent of cell volume (124).
In walled organisms such as algal cells, changes in membrane structure have been proposed to be responsible for
activating turgor-regulating processes. Zimmerman et al.
INVITED
Cl67
REVIEW
Ca2+
Pathway
Cell
K+-H+ exchange
Taurine
efflux
K+ conductance
Protein
kinases
Leukotrienes
Cyclic AMP
Cl- conductance
Na-H
exchange
Na+-H+
exchange
Taurine
efflux
K+ and Cl- conductances
Na+-H+
and Cl--HCO,
exchangers
Types
Amphibian
red blood cells
Molluscan
red blood cells
Elasmobranch
red blood cells
Amphibian
gallbladder
Amphibian
urinary
bladder
Ehrlich
ascites cells
Lymphocytes
Ehrlich
ascites cells
Lymphocytes
Lymphocytes
Elasmobranch
red blood cells
Ehrlich
ascites cells
Mammalian
renal cells
Refs.
31
141
101
52,54
33,42
82
65
82
64
66
111
96
73, 74
Cl68
INVITED
REVIEW
by external hypertonicity
(87). Cairney et al. (30) and
Dunlap and Csonka (45 ) have demonstrated that expression of the proU gene that encodes for a high-affinity
betaine transport system is dramatically
increased in S.
typhimurium
within minutes after exposure to hyperosmotic media. A proline and betai ne transport system
encoded for by the prop ge ne is induced in both S.
typhimurium
(29) and E. coli (60,87). In E. coli a choline
uptake system is induced by hypertonicity
as well (147).
Choline is converted to betaine in these organisms bY
the action of two dehydrogenases : ch .oline dehydrogen .ase
and glycine betaine aldehyde dehydrogenase. Both enzymes are induced in osmotically stressed cells (97) .
As discussed earlier, the Kdp system is partially responsible for osmoregulatory
K+ uptake in E. coli. -This
transport system is dependent on the expression of five
closely linked genes (reviewed in Ref. 47). Three inner
membrane proteins are encoded by the kdpA, kdpB, and
kdpC genes, which form an operon. Two positive regulators of these genes are encoded for by the adjacent
kdpDE operon. Laimins
et al. (95) have conducted a
series of elegant studies on the induction of the Kdp
system. The results of these investigations demonstrated
that neither alterations in intracellular
or extracellular
K+ affected gene expression unless external K+ dropped
to a point that limited cell growth. When external osmolality was increased at constant K .+ using impermeant
solutes, however, kdpABC expression was increased. Elevation of extracellular osmolality with the highly membrane permeable solute, glycerol, had no effect on expression. These results demonstrate that hypertonici .ty with
associated decreases in turgor pressure increases the
transcription
of the kdpA&operon.
The mechanisms
by which these diverse bacterial
genes are controlled by external osmolality are not completely understood. Several intriguing models have, however, been put forth. Epstein and co-workers (47, 95)
have postulated a mechanogenetic
control mechanism.
Studies by these investigators on the Kdp system have
indicated that the kdpD gene encodes -for a 70-kDa
protein that spans the periplasmic space, whereas kdpE
encodes for a 26-kDa soluble protein. The kdpD protein
1Medium
Osmolality
\1
\1 Turgor
I
d
?i&@
expression
? Intracellular
K+
? Betaine
& uptake
fTuY!gor
FIG. 1. Proposed
control of gene expression
during turgor regulation
in eubacteria.
Decreased
turgor
stimulates
ka! expression
and K+
accumulation.
Increased
intracellular
K+ stimulates
proU expression
and inhibits
kdp expression.
See text and Refs. 47, 75, 148 for detailed
descriptions
of these events.
INVITED
Maintenance
of cell volume in the face of a changing
osmotic environment
was a physiological
problem faced
by the earliest life forms. It seems reasonable, therefore,
to hypothesize
that there are common mechanisms
underlying volume regulatory
processes
in extant organisms. It has been difficult,
however, to confirm this
hypothesis
in this review since specific aspects of cell
volume regulation have been studied in only a few species. Throughout
this article we tried to indicate areas
that may be particularly
important in understanding
the
mechanisms and control of cell volume regulation in all
organisms.
All cells experiencing
osmotic stress must
have some means of sensing their volume so that they
can initiate mechanisms
to adjust their intracellular
osmolality. The nature of these sensors and the level of
their sensitivity
are poorly understood, and further work
in this area is clearly needed. The intracellular
signals
that activate volume regulatory responses are just beginning to be explored, and this promises to be an exciting
area of research. Genetic aspects of cell volume regula-
REVIEW
Cl69
tion have been examined in bacteria, but an understanding of the role of the genome in eucaryotic cell volume
regulation is in its infancy. The coordinated use of inorganic and organic osmolytes during cell volume regulation deserves more attention, and the effect of fluctuating
osmolyte concentrations
on cellular metabolism needs to
be explored. Solute effects on protein structure and function have been investigated,
but these studies should be
expanded and the biological consequences
of proteinsolute interactions
need to be elucidated.
A coherent picture of the evolutionary,
physiological,
metabolic, and environmental
constraints
on the mechanism of cell volume regulation employed by a particular
species is dependent on a better understanding
of this
process in a wide variety of organisms.
It is hoped that
this review will stimulate
more studies on cell volume
regulation and has served to emphasize the value of a
comparative
approach to cellular physiology.
We wish to thank
Drs. J.S. Ballantyne,
M.A. Bisson,
J.H. Crowe,
S.R. Gullans,
S.H. Hebert,
and P.K. Lauf for their helpful comments
during the preparation
of this review.
This work was supported
in part by National
Institute
of Diabetes
and Digestive
and Kidney
Diseases
Grant DK-37317
and funds from
the Ohio University
College of Osteopathic
Medicine.
Address for reprint
requests: M. E. Chamberlin,
Dept. of Zoological
and Biomedical
Sciences,
Irvine
Hall, Ohio University,
Athens,
OH
45701.
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