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Intra- and Extracellular Dehydration Has No Effect
on Plasma Levels of Angiotensin II in an Amphibian
Northern Arizona University, Department of Biological Sciences, Flagstaff,
Arizona 86001
Previous studies have demonstrated that both dehydration (intra and extracellular) and treatment with angiotensin II (A-II) induce changes in thirst-related behavior in the
spadefoot toad, Scaphiopus couchii. One of the steps in determining a causal relationship between
a hormone and a behavior is to determine that there is association between an animal’s performance of the behavior and changes in endogenous hormonal concentrations. The hypothesis tested
that plasma levels of the peptide hormone A-II would change as a result of dehydration known to
induce water absorption response (WR) behavior in the spadefoot toad. Plasma samples were taken
from toads dehydrated intracellularly by injection of hypertonic solutions of NaCl or sucrose at
levels known to induce WR behavior. As an osmotic control, a group of animals was injected with
urea, which has been demonstrated to not induce WR behavior. In order to determine the effects
of extracellular dehydration on plasma, A-II levels in toads dehydrated by plasma volume depletion via cardiac puncture were compared to sham-punctured controls. None of the treatments in
any experiment resulted in significant differences in plasma levels of angiotensin II among groups
sampled at the time when WR behavior occurs. These results do not support the hypothesis that
dehydration-induced thirst is stimulated by changes in plasma A-II concentrations at the onset of
WR behavior. J. Exp. Zool. 286:343–349, 2000. © 2000 Wiley-Liss, Inc.
Drinking is the primary behavioral response to
dehydration for most vertebrates (Grossman, ’90).
An understanding of the physiological mechanism
that initiates drinking behavior is key to understanding how terrestrial vertebrates avoid debilitating dehydration. Fish, reptiles, birds, and
mammals rehydrate through oral intake of fluids. However, in anuran amphibians, water is
taken in across the ventral seat patch as an animal abducts its hind limbs and presses the pelvic
region to a wet substrate (Stille, ’52; Bentley and
Yorio, ’79). This behavior is termed water absorption response (WR) by Brekke et al. (’91) and can
be induced by denying animals access to water
(Brekke et al., ’91; Propper and Johnson, ’94). Although the behavior in amphibians is different
from most other taxa, water-obtaining behavior
is still elicited by dehydrating conditions.
Primary drinking behavior is initiated by dehydration (Fitzsimons, ’79). Dehydration may occur
as a result of intracellular loss of fluids or fluid
depletion of the extracellular space. For example,
when water is removed from cells (intracellular
dehydration) or plasma volume is decreased (extracellular dehydration), oral drinking behavior
is induced in dogs (Gilman, ’37; Bellows, ’39), rats
(Adolph et al., ’54; Fitzsimons, ’61; Ramsay et al.,
’76; Janczewski et al., ’87; Salisbury and Rowland,
’90; Stricker ’91), mice (Rowland and Fregly, ’88),
reptiles (Fitzsimons and Kaufman, ’76) and amphibians (Bentley and Yorio, ’78; Brekke et al.,
’91; Taylor et al., ’99). Intracellular dehydration
can be induced experimentally by administration
of hypertonic solutions to an animal, thus increasing the osmotic gradient outside the cell resulting in intracellular dehydration. Intracellular
dehydration induced by treatment with hypertonic
saline solutions leads to drinking behavior. Although the specific behavioral response is different in anuran amphibians, again, treatment with
hypertonic solutions initiates drinking (cutaneously). When water is removed from cells (intracellular dehydration), an increase in WR behavior
is observed in the spadefoot toad Scaphiopus
couchii (Taylor et al., ’99). In these studies, dehydration was induced by administration of solutions
hypertonic to the animal, which increases the osmotic concentration in the extracellular space reGrant sponsor: National Science Foundation; Grant number: IBN
*Correspondence to: Loretta P. Mayer, Northern Arizona University, Dept. of Biological Sciences, P.O. Box 5640, Flagstaff, AZ 86001.
Received 1 December 1998; Accepted 20 July 1999
sulting in an osmotic gradient that induces intracellular dehydration. Treatment with urea,
which passes freely across the cell membrane and
does not create an osmotic gradient, was ineffective in inducing any significant increase in WR
Voluntary water intake has also been observed
following extracellular dehydration resulting from
a depletion of blood volume. In rats, a blood volume reduction of one-third induced an oral drinking response (Ramsay et al., ’76; Stricker, ’91). In
iguanas, extracellular dehydration induced by injection of hyperoncotic polyethylene glycol caused
a significant increase in drinking when compared
to vehicle injected controls (Fitzsimons and Kaufman, ’76). These studies demonstrate that multiple
forms of dehydration induce behavioral rehydration
response across many taxa. Extracellular dehydration as a result of a reduction in blood volume has
also been observed to be a stimulant of WR behavior in amphibians by Taylor et al. (’99).
The specific signals that precipitate WR behavior are unclear. It has been suggested that the
hormone angiotensin II (A-II) is an important
dipsogen in other taxa (Epstein et al., ’70; Fitzsimons and Kaufman, ’76; Kobayashi et al., ’78;
Gray and Erasmus, ’88; Wright et al., ’88; Volmert
and Firman, ’91). Again, although the behavioral
response is different, A-II also initiates WR behavior in amphibians (Hoff and Hillyard, ’91;
Propper and Johnson, ’94; Propper et al., ’95;
Hillyard et al., ’98). These studies demonstrated
that administration of exogenous A-II resulted in
a significant increase in WR behavior. The results
of these studies suggest that plasma levels of AII may change with the hydration state of the animal, and that these changes may play a role in
the induction of behavior.
To determine if the role of plasma A-II is causal
in the induction of WR behavior, it is necessary
to establish that there is an association between
the animal’s performance of the behavior and
changes in endogenous plasma hormone concentrations. This study investigates whether intracellular and or extracellular dehydration induces
changes in plasma levels of A-II in the spadefoot
toad, Scaphiopus couchii.
Prior to each experiment, the animals were
weighed, then hydrated in dechlorinated tap water for 3 hr. Following this hydration period, the
toads were again weighed, their bladders were
emptied by cloacal cannulation with a small pipet tip, and they were weighed again before receiving treatment. Because toads can reabsorb
water from the urinary bladder and this reabsorption is increased during dehydration, it is necessary to control for this condition by using animals
with empty bladders (Ruibal, ’62). The vehicle for
the intraperitoneal injections was amphibian
Ringer’s (115 mM NaCl, 2.5 mM KHCO3, 1.0 mM
CaCl2; pH 8.0) at 20.0 µl/g toad. After injection,
the animals were placed in a dry plastic box (30 ×
15 × 10 cm) for 30 min. Following the 30-min period, the toads were weighed and blood samples
collected by cardiac puncture for hormone and osmolarity measurements. Toads were weighed
again and returned to the 10-gallon tanks with 1
liter of dechlorinated tap water to rehydrate for 1
hr prior to being returned to their storage boxes.
For experiment 1, toads (n = 8) were treated
with (a) Ringer’s (b) Ringer’s + 0.5 M NaCl, and
(c) Ringer’s +1.0 M NaCl. In experiment 2, toads
(n = 7) were treated with (a) Ringer’s, (b) Ringer’s
+ 0.5 M sucrose, and (c) Ringer’s + 1.0 M sucrose.
These doses have been demonstrated previously
to induce WR behavior in this species (Taylor et
al., ’99). In experiment 3, toads (n = 7) were
treated with (a) Ringer’s and (b) Ringer’s + 1.7 M
urea. All toads received all treatments in random
order over the course of the experiment. Toads
never received more than one treatment during
any given week.
Extracellular dehydration
Scaphiopus couchii were collected from the
Buenos Aires Wildlife Refuge, Pima County, Arizona, during the monsoon season (June–July) in
1996. The animals were transported to the laboratory in large containers (53 × 41 × 18 cm) that
Toads (n = 10) were initially weighed and hydrated in dechlorinated tap water for 3 hr. Following this hydration period, the toads were
bladder emptied by cloacal cannulation with a
small pipet tip, and weighed again before receiv-
contained 15 cm of loose peatmoss and water ad
libitum. Approximately 10 toads (weight range,
14–30 g), were stored in each container. Once in
the laboratory, the toads were transferred, one
toad per container, to a plastic box (30 × 15 × 10
cm) containing 7 cm soil, and water was available ad libitum. The animals were fed crickets
three times a week. The room was maintained at
a temperature of 25°C and a 12 hour light:12 hour
dark photoperiod.
Intracellular dehydration
ing treatment. A 0.5-cc syringe with a ½ inch, 25gauge heparinized needle was used for the heart
puncture procedure. For experiment 4, the animals received (a) a sham puncture into the pericardial space with no blood removed or (b) a
cardiac puncture through which 127.3 ± 10.4 (x
SE) µl of blood was removed. After treatment, the
animals were placed in a dry plastic box (30 × 15
× 10 cm) for 30 min. Toads were then weighed,
sampled, weighed, and rehydrated as previously
For each experiment, each individual received
all treatments. There was a minimum of one week
between each treatment regimen.
Hormone measurements
Hormone levels were assayed using a fluid
phase radioimmunoassay (RIA). Samples were collected in peptidase inhibitor described by Ledwith
et al. (’93). The RIA was based on the technique
described by Hanssens et al. (’90). Briefly 125I-labeled A-II (Ile5) (specific activity = 2 × 106 µCi/
µMole), purchased from Amersham (Buckinghamshire, England), was suspended in 10 mM K2HPO4,
1 mM EDTA, 0.1% gelatin (P-gel buffer) buffer, pH
7.3, and incubated with rabbit A-II antiserum
(Peninsula Laboratories, Inc., Belmont, CA) in Pgel buffer. Antiserum titer used was 1:100,000,
and cross-reactivity with AIII was 100%, and results are reported as immunoreactive angiotensin
(irANG) concentrations. Unbound label was separated from bound with a dextran/charcoal slurry.
A Beckman LS5000TD gamma counter was used
to detect the bound hormone-antibody complex.
Serum concentrations of total angiotensin (AII and
AIII) were calculated from premeasured standards
(0.95–500 pg/100 µl) using four-parameter logistic analysis of the data using Assay-Zap software
(Biosoft, Ferguson, MO). All samples within each
experiment were run in the same assay. The limit
of detection for the assay was 1.9 pg/100 µl with
an intraassay cv of 11.29% (n = 10). A five-point
serial dilution of S. couchii plasma was determined to be parallel to the standard curve.
Osmolarity measurements were determined
by vapor pressure osmometry using a Wescor
5500. During the collection of data, the osmometer was recalibrated every 20 samples with
100, 290, and 1000 mmole/kg standards to
eliminate drift in the readings. Osmolarity measurements were taken from plasma samples
following hormone measurement. Due to an insufficiency of plasma collected from some individuals, not all animals were measured.
Data analysis
The differences in plasma concentrations of angiotensin and osmolarity measurements among
treatments were analyzed using a one-way repeated measures ANOVA for experiments 1 and 2
and a paired t-test for experiments 3 and 4. The
functional relationships between plasma hormone
levels and osmolarity were analyzed by linear regression.
Intracellular dehydration
Experiment 1
Sodium chloride treatment did not induce any
significant changes in plasma levels of irANG (Fig.
1a; n = 8, P = 0.772). Osmolarity measurements
among the three treatments were not significantly
different (Table 1; n = 5, P = 0.652). There was no
correlation between plasma irANG levels and osmolarity measurements in any of the NaCl treatment groups (Table 2; n = 5).
Experiment 2
Sucrose treatment also did not induce any significant changes in plasma levels of irANG (Fig.
1b; n = 7, P = 0.068). Osmolarity measurements
among the treatment groups were not significantly
different (Table 1; n = 4, P = 0.215). There was no
functional relationship between plasma irANG
levels and osmolarity measurements in any of the
sucrose treatment groups (Table 2; n = 4).
Experiment 3
Treatment with urea had no significant effect
on plasma levels of irANG (Fig. 1c; n = 7, P =
0.956). Osmolarity measurements among the
treatment groups were not significantly different
(Table 1; n = 6, P = 0.104). There was no functional relationship between plasma irANG levels
and osmolarity measurements in any of the urea
treated groups (Table 2; n = 6).
Extracellular dehydration
Experiment 4
Depleting blood volume by heart puncture did
not cause any significant changes in plasma levels of irANG (Fig. 1d; n = 10, P = 0.181). Osmolarity measurements among the treatment groups
were not significantly different (Table 1; n = 8, P
= 0.407). There was no functional relationship between plasma irANG levels and osmolarity measurements in any of the treatment groups (Table
2; n = 8).
Fig. 1. Plasma irANG concentrations following treatments
with increasing doses of osmolytes or cardiac puncture in male
S. couchii. (a) NaCl treatments; n = 8; P = 0.772; (b) sucrose
treatments; n = 7; P = 0.068; (c) urea treatment; n = 7; P =
0.956; (d) blood volume reduction; n = 10; P = 0.181. Bars
represent the mean for each treatment group ± SEM. No
treatment resulted in changes in plasma irANG.
however, was not significantly different from the
other two groups. The plasma osmolality for the
second group was significantly elevated over animals in group 3, and there was no difference in
plasma irANG between the three groups. Brain
levels of irANG did differ among the groups in
the periventricular nucleus. Animals displaying
WR behavior had higher levels than those in the
other two groups (Johnson, ’97). These data support the possibility that the role of A-II in amphibian thirst behavior may be a central one.
Laboratory animals dehydrated by 5, 10, and
15% of their standard weight also did not have
significantly different plasma levels of irANG compared with fully hydrated controls, even though
animals dehydrated by 15% of their standard
weight demonstrated significantly higher WR behavior from the other groups (Johnson, ’97). In
these studies, the toads that were dehydrated by
15% had significantly higher plasma osmolalities
when compared with controls. These data are
similar to the results reported here in that dehy-
Both intracellular and extracellular dehydration
treatments known to induce WR behavior (Taylor
et al., ’99) were ineffective in inducing any significant change in circulating plasma levels of
irANG. Further, these treatments did not significantly elevate the osmolarity of circulating plasma. These results are consistent with other
studies in amphibians. Plasma irANG measurements of spadefoot toads exhibiting WR behavior
in field conditions were not significantly different
from toads exhibiting breeding behavior or other
activities (Johnson, ’97).
In the field study of Johnson (’97), animals were
collected during one of three behaviors: (1) displaying WR behavior on the first two nights of
the monsoon rains, (2) active on the roadway not
in WR behavior on nights 3 and 4, and (3) in a
breeding pond on the fourth night. The animals
in the first group were presumed to be displaying
WR behavior to rehydrate following their lengthy
estivation. The plasma osmolality for this group,
TABLE 1. Effects of different dehydration treatments across
all experiments on plasma osmolarity in S. couchii
Mean osmolarity
following treatment
(±SE) mmol/kg
0 M NaCl
0.5 M NaCl
1.0 M NaCl
0 M sucrose
0.5 M sucrose
1.0 M sucrose
0 M urea
1.7 M urea
Sham puncture
Cardiac puncture
P value (repeated
measures ANOVA)
274.6 (±5.64)
284.6 (±20.87)
291.0 (±12.46)
264.3 (±15.7)
314.0 (±27.7)
283.7 (±11.1)
263.8 (±13.2)
251.2 (±7.53)
283.4 (±14.45)
272.8 (±6.81)
drating conditions sufficient to induce WR behavior, and animals performing WR behavior in field
conditions and the laboratory, do not have altered
levels of plasma irANG when compared to hydrated individuals.
Studies in rat are also consistent with these
findings relative to plasma levels of A-II. Intravenous infusion of A-II (10–200 ng/kg/min) resulted
in a drinking response that increased in a dosedependent manner to 100 ng/kg/min, then leveled
off. The response to the highest dose was observed
within eight min, and plasma levels of A-II for doses
above 50 ng/kg/min were equivalent to plasma A-II
levels after 48 hr of dehydration, however, there
were no significant differences among A-II treated
TABLE 2. Correlation of plasma levels of irANG
and plasma osmolarity following each dehydration
treatment in S. couchii
0 M NaCl
0.5 M NaCl
1.0 M NaCl
0 M sucrose
0.5 M sucrose
1.0 M sucrose
0 M urea
1.7 M urea
Sham puncture
Cardiac puncture
Correlation of plasma
levels of irANG and
osmolarity following
treatment (r2)
F value (linear
groups at the onset of drinking behavior, which is
achieved with the minimal (50 ng/kg/min) dose of
A-II, indicating a threshold relationship may exist
(Anke et al., ’88). These studies suggest that A-II
plays a role in stimulating drinking behavior only
when dehydration is severe.
To investigate the potential dipsogenic role of
A-II, studies have been conducted to compare
methods of administration of exogenous A-II and
their resultant effects on WR behavior. Induction
of WR behavior by intracerebroventricular (icv)
injection of A-II in the spadefoot toad was reported
at 10 ng (Propper et al., ’95). This dose is approximately 1,000-fold less than the dose necessary to
induce behavior via intraperitoneal (ip) injection
in the same species (Propper and Johnson, ’94).
These studies suggest that A-II may be functioning as a neurotransmitter in the induction of WR
behavior in anurans, and that plasma A-II may
not be a factor in generating a thirst response in
this species.
Recent studies on A-II induced gene expression
addresses the potential role of A-II as a neurotransmitter with associated behavioral changes.
Extracellular dehydration following hemorrhage
in rats resulted in an increase in the production
of Fos, a marker of cell activation and c-fos, an
early-response gene, in the subfornical organ, organum vasculosum of the lamina terminalis, supraoptic and paraventricular nuclei (Badoer et al.,
’93). Further studies showed that icv injections of
A-II resulted in intense staining for c-fos in the
median preoptic nucleus, organum vasculosum,
subfornical organ, paraventricular nucleus, and
supraoptic nucleus (Mahon et al., ’95). The expectation that this gene expression was a result of
an increase in A-II was supported by the expression of c-fos following stimulation of the AT1 receptor in the midbrain and brainstem of rats that
were treated with icv A-II (Lebrun et al., ’95).
Mahon et al. (’95) subsequently observed similar
increases in c-fos expression that correlated with
an increase in drinking behavior. Further investigation of the potential mechanism of the A-II
neurotransmission involved in drinking has shown
mitogen-activated protein kinase (MAPK), an important signaling pathway for the stimulation of
c-fos like genes, to be upregulated in rat neuronal
cultures stimulated with A-II (Lu et al., ’96). These
studies are the first to demonstrate this downstream signaling pathway in A-II-mediated neuromodulation in noradrenergic neurons. Studies
of the kinetics of the A-II induced expression of cfos in vitro have shown that once c-fos expression
is initiated, the process becomes independent of
the hormone-receptor interaction (Garcia-Sainz et
al., ’95), suggesting that plasma levels of A-II may
spike to a threshold level necessary for induction
of the signaling cascade and then recede to
prestimulated levels. These studies, in total, support the hypothesis that the role of A-II in the
initiation of a water response behavior as a result of dehydration occurs centrally. Therefore,
changes in plasma levels of A-II would not necessarily be observed following, or even concurrent
with, the performance of the behavior. This is consistent with observations in a natural field population of male S. couchii performing WR behavior
at the onset of the monsoon season wherein levels of A-II in the periventricular nucleus of the
hypothalamus were elevated over active or breeding toads. The irANG concentrations in the PVN
of these animals did not correlate with plasma
angiotensin concentrations (Johnson, ’97).
Another possibility is that desert anurans are
relatively insensitive with respect to an A-II response to moderate dehydration levels. Studies of
birds have shown that plasma levels of A-II increase three-fold with a significant correlation in
osmolality and drinking behavior following severe
dehydration by water deprivation (Gray and
Erasmus, ’88). Birds were water deprived for 3–5
days to induce a 5% reduction in standard weight.
This amount of reduction in standard weight for
this species is considerable and amounts to severe dehydration, whereas a reduction in standard
weight of desert anurans of up to 45% can be tolerated. These studies suggest that dehydration
induces an increase in plasma levels of A-II following severe dehydration and that this increase
is positively correlated with osmolality that reflects the decrease in both intra- and extracellular water, and drinking that occurs following these
levels of dehydration may be associated with
plasma levels of A-II. This presents the possibility that A-II may play a role in dehydration-induced drinking when dehydration levels are
severe. Spadefoot toads have survived dehydration of up to 45% of their standard weight. Therefore, dehydration levels of 15% in the spadefoot
toad, are by comparison not extreme and would
not fall into the severe category.
We thank Dr. Cheryl Dyer for her continued
technical assistance and support. We also thank
Stan Hillyard, Bill Johnson, and Randy Wade for
their comments. A special thank you goes to Mr.
Manuel Santana for his assistance in collecting
the animals and Kim Epand for excellent animal
care. The staff of the U.S. Fish and Wildlife Service at the Buenos Aires Wildlife Refuge has been
consistently helpful and courteous hosts. This
work was supported by NSF grant IBN 93-10352
to C.R. Propper.
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