In vertebrates, the renin–angiotensin system (RAS) plays an
important role in the control of hydromineral balance and
blood pressure regulation (Robertson, 1993). The main
vasoactive component of the RAS is angiotensin II (AngII),
although angiotensin I (AngI) and truncated forms may also
have biological effects in mammals (Head and Williams,
1992). AngII is cleaved from AngI by the action of
angiotensin-converting enzyme (ACE) and exerts its biological
action by means of specific membrane receptors; two main
subtypes, AT1 and AT2, have been identified so far in
mammals (Wright and Harding, 1994). In mammals, saralasin
specifically antagonises the action of AngII at the receptor
level, although it may have a partial agonist effect in some
models. In vivo it causes lowering of blood pressure only when
the RAS is pre-activated (Moore and Fulton, 1984).
All the components of the RAS have been identified in fish
(Olson, 1992; Takei, 1993) but, despite attempts to understand
its role, the physiological action of the RAS in fish is far from
fully understood. The stimulation of the endogenous RAS by
increases in external salinity, elevation of blood plasma ionic
concentration, dehydration, blood volume depletion or lowered
blood pressure is the major stimulus for the development of the
drinking response, which compensates for osmotic loss of
water from fish in sea water (Balment and Carrick, 1985;
Takei, 1993; Tierney et al. 1995; Fuentes et al. 1996). The
exogenous administration of components of the RAS, e.g.
AngI and AngII, also results in increased drinking rates in both
freshwater- and seawater-adapted fish (Perrot et al. 1992;
Fuentes and Eddy, 1996), a response antagonised by saralasin
(Fuentes and Eddy, 1996); however, saralasin was without
effect on the blood pressure response to AngII in eel (Anguilla
rostrata) and sculpin (Myoxocephalus octodecimspinosus) in
sea water (Nishimura et al. 1978; Carroll, 1981) and in
freshwater rainbow trout O. mykiss (Conklin and Olson,
The contribution of the RAS to blood pressure regulation
has recently been demonstrated in a series of elegant studies
based on cardiovascular preparations, and can be summarised
as follows: (i) although AngII is a potent vasoconstrictor in
perfused systemic tissues in trout, there is little contractile
activity in large blood vessels in vitro (Conklin and Olson,
1994a); (ii) there is a triphasic response to AngII in
precontracted large blood vessels, with an initial small and
transient contraction followed by a large relaxation, before
recovery (Conklin and Olson, 1994b); and (iii) the
microcirculation is the most important target for AngII pressor
responses (Olson et al. 1994), and the venous system is not an
important target of the RAS (Zhang et al. 1995).
There have been few in vivo cardiovascular studies
involving AngII in fish and, although the response of heart rate
The Journal of Experimental Biology 201, 267–272 (1998)
Printed in Great Britain © The Company of Biologists Limited 1998
The effects of [Asn1,Val5]-angiotensin II (AngII) and
[Sar1,Val5,Ala8]-angiotensin II (saralasin) on dorsal aortic
blood pressure, pulse pressure and heart rate were
examined in rainbow trout in vivo. AngII when
administered as a single dose of 25µgkg−1induced a
biphasic response in blood pressure, with a significant
hypertensive response during the initial 10min, followed by
a significant hypotension of 70–75% compared with the
initial blood pressure after 50min and continuing until
administration of AngII (25µgkg−1) and saralasin
(50µgkg−1) resulted in the same hypertensive response
during the initial phase, but abolished the hypotensive
effect of AngII. Heart rate was significantly increased in
post-injection. The co-
response to AngII, but the administration of AngII and
saralasin together attenuated
approximately 44%. Stimulation of the endogenous
renin–angiotensin system using a vasodilator, sodium
nitroprusside, significantly increased drinking rate in
rainbow trout fry, a response inhibited by saralasin,
indicating a role for AngII-induced hypotension in
drinking. For the first time, a decrease in blood pressure in
response to AngII in vivo has been demonstrated in fish,
and this is discussed in relation to homeostasis of blood
pressure and a possible role in the control of drinking.
the increase by
Key words: trout, Oncorhynchus mykiss, renin–angiotensin system,
cardiovascular, blood pressure, hypotension, drinking.
CARDIOVASCULAR RESPONSES IN VIVO TO ANGIOTENSIN II AND THE PEPTIDE
ANTAGONIST SARALASIN IN RAINBOW TROUT ONCORHYNCHUS MYKISS
JUAN FUENTES AND F. BRIAN EDDY*
Department of Biological Sciences, University of Dundee, Dundee DD1 4HN, Scotland, UK
*Author for correspondence (e-mail: email@example.com)
Accepted 31 October 1997: published on WWW 22 December 1997
among species was variable, all studies demonstrated a short-
term hypertensive effect, lasting approximately 10min (cod
Gadus morhua, Platzack
borchgrevinki, Axelsson et al.1994; rainbow trout O. mykiss,
Olson et al. 1994; Le Mevel et al. 1994; eel Anguilla anguilla,
Oudit and Butler, 1995b). The aim of the present work was to
examine cardiovascular responses to exogenous AngII and
saralasin in trout in order to explore the possibility that changes
in blood pressure are involved in the drinking response.
Materials and methods
Adult and fry rainbow trout [Oncorhynchus mykiss
(Walbaum)] of either sex were obtained from College Mill
Trout Farm in Perthshire, Scotland, UK, and reared at Dundee
University Aquarium for at least 2 weeks before experiments.
Mean values of freshwater quality (mmoll−1) were: Na+, 0.19;
K+, 0.02; Ca2+, 0.24; Mg2+, 0.07; Cl−, 0.03; free CO2, 0.02;
alkalinity as CaCO3, 20.5mgl−1; total hardness as CaCO3,
31.3mgl−1; non-bicarbonate hardness as CaCO3, 10.6mgl−1;
pH8.2; the temperature was 9–11°C, the temperature for all
procedures unless otherwise stated.
Rainbow trout (250–350g) were anaesthetised in 3-
aminobenzoic acid ethyl ester (Sigma, 1:25000 neutralised
with NaHCO3), weighed and transferred to an operating table.
The gills were perfused constantly with aerated water
containing a neutralised anaesthetic solution (1:50000) and
then chronically fitted with an indwelling cannula (Portex, i.d.
0.58mm, o.d. 0.96mm) in the dorsal aorta according to
previous methods (Soivio et al. 1972). After surgery, the
cannulae were filled with heparinized Cortland fish saline, and
the fish were transferred to 5l darkened plastic boxes with
flowing aerated water (0.5lmin−1). Fish were allowed to
recover for 72h before performing any procedure, and
the cannulae were flushed daily with heparinized fish saline
(30i.u.ml−1, sodium heparin, Sigma).
[Asn1,Val5]-angiotensin II (acetate salt, Sigma) was diluted
in fish saline to give final doses of 25µgkg−1. [Sar1,Val5,Ala8]-
angiotensin II (saralasin, Sigma) was prepared as above to give
a final dose of 50µgkg−1. The doses of AngII and saralasin
were selected according to previous studies on drinking
responses (Fuentes and Eddy, 1996), according to preliminary
experiments (data not shown) and according to the range used
previously in vitro (Conklin and Olson, 1994b; Olson et al.
1994) and in vivo (Axelsson et al. 1994; Olson et al. 1994).
Saline composition was as follows (mmoll−1): NaCl, 124.1;
CaCl2.2H2O, 1.4; KCl, 5.1; Na2HPO4.H2O, 2.9; NaHCO3,
11.9; MgSO4.7H2O, 1.9 and glucose, 5.6, pH7.5 (Houston et
al. 1985), administered at the experimental temperature. The
peptides, freshly prepared in 200–300µl of fish saline, were
slowly delivered over a period of 3min via the cannula without
physical disturbance to the fish, and dorsal aortic pressure
recordings were taken initially at 5min and then at 10min
intervals over a period of 90min.
Blood pressure, pulse pressure and frequency were
monitored using a Washington PT 400 pressure transducer
attached to a Washington oscillograph 400 MD/211, using a
static column of water as a standard. Recordings were taken
for at least 30min before and 90min after administration of
the peptides. Recorded traces were used to calculate heart
rate (beatsmin−1), mean
[(systolic+diastolic)/2] (Olson et al. 1994) and pulse pressure
(systolic minus diastolic). Blood pressure and pulse pressure
were expressed in kPa, and all values are presented as mean
arterial blood pressure
Drinking rate was measured as described previously
(Fuentes and Eddy, 1996). In brief, groups of rainbow trout fry
(2–3g) were placed in 400ml of aerated fresh water in
darkened plastic boxes (13–15°C) with approximately
30–40kBq 51Cr-labelled EDTA (Amersham) to give an
activity of approximately 2000ctsmin−1ml−1(Wallac gamma
counter). At the end of the experiments (3h), fish were killed
by an overdose of benzocaine (400mgl−1), gently blotted dry
and kept at −20°C until frozen (1h), then weighed and quickly
dissected before thawing. The guts were transferred to a tube
for radioactivity counting. Drinking rates were expressed as
To establish whether changes in blood pressure induced by
AngII were involved in the drinking response, drinking rates
were measured, following the methods of Fuentes and Eddy
(1996), in trout fry (2–3g) in response to (1) a 10µl
intramuscular injection of fish saline; (2) a saline injection plus
the addition of 1.5mmoll−1of the vasodilator sodium
nitroprusside to the water (McGeer and Eddy, 1996; Fuentes
et al. 1996); (3) the addition of 1.5mmoll−1sodium
nitroprusside in the water plus an intramuscular injection of
3µgg−1saralasin (Sigma); and (4) intramuscular injection of
Comparisons between means were performed using analysis
of variance (ANOVA) (two-way and one-way followed by
Dunnet’s test) after testing for normality (Kolmogorov–
Smirnov’s test) and homogeneity of variances (Cochran’s test).
Differences between means were considered significant at
P<0.05, unless stated otherwise.
Measurement of dorsal aortic blood pressure for at least
30min in untreated conscious rainbow trout gave steady values
of approximately 3.7kPa, and administration of AngII resulted
J. FUENTES AND F. B. EDDY
AngII and cardiovascular responses in trout
in a biphasic response in blood pressure (Fig. 1). After the
administration of AngII (25µgkg−1), hypertension occurred,
reaching a maximum after 5min, an increase of approximately
80% (Fig. 1) with respect to pre-injection values, followed by
a rapid decrease towards control levels in the next 10min.
Subsequently, blood pressure showed a slower, but continuous,
decrease until 50min following injection, when it was
significantly (P<0.05) lower than pre-injection values (Fig. 1).
This period of hypotension lasted between 50 and 80min post-
injection, with values of approximately 2.7kPa, about 70% of
the initial blood pressure.
The hypertensive response to AngII administration was not
inhibited by the co-administration of saralasin (50µgkg−1),
and the increase in blood pressure resembled the response to
AngII alone (Fig. 1). However, the hypotensive response to the
administration of AngII was not obtained in presence of
saralasin (Fig. 1). Blood pressure decreased to pre-injection
levels after 10min, then declined to approximately 90% of
control values, and reached a minimum value of approximately
85% at 80min (Fig. 1). These decreases were not significantly
different from pre-injection values.
Table 1 shows pulse pressure dynamics in response to AngII
and to co-administration of AngII and saralasin. Both
treatments produced the same response with a significant
(P<0.01) increase 5min after administration of the peptide(s),
followed immediately by a return to pre-injection values which
continued for the duration of the measurements.
As shown in Fig. 2, AngII induced a significant (P<0.001)
increase in heart rate of approximately 60% (between 40% and
Blood pressure (kPa)
AngII + saralasin
Fig. 1. Dorsal aortic blood pressure (kPa) in rainbow trout in response
to a bolus injection of AngII (25µgkg−1) (open circles). The response
to a bolus injection of AngII (25µgkg−1) plus saralasin (50µgkg−1)
(filled triangles) is also shown. Values for at least 30min preceding
injection are shown, and the peptide was administered at time 0.
Significant increases or decreases are shown with respect to pre-
injection values (**P<0.01, *P<0.05). Values are means ± S.E.M. of
six fish for each treatment.
Table 1. Pulse pressure in rainbow trout before (pre-
injection) and after the administration of angiotensin II
(AngII) or AngII and saralasin
Pulse pressure (kPa)
AngII (25µgkg−1) or AngII (25µgkg−1) plus saralasin (50µgkg−1).
Values are shown as means ± 1 S.E.M. (N=6 for each treatment);
**significant (P<0.01) difference from pre-injection values (one-way
Fig. 2. Heart rate (beatsmin−1) in response to a bolus injection of
AngII (25µgkg−1) (open circles) or AngII (25µgkg−1) plus saralasin
(50µgkg−1) (filled circles). The administration of the peptides is
represented by the arrow. Significant differences are shown with
respect to pre-injection values (***P<0.001, **P<0.01, *P<0.05).
Values are represented as means ± S.E.M. of six fish for each treatment.
Treatments are significantly different (P<0.001, F=8.357, two-way
Heart rate (beatmin−1)
0 15 30456075 90
70%) throughout the experimental period. The co-
administration of saralasin and AngII resulted in a smaller
increase in heart rate, of approximately 44% (between 35%
and 48%) compared with pre-administration levels, which was
significantly different from both control values and AngII
values (P<0.001, F=8.357, two-way ANOVA).
Rainbow trout fry drank at a rate of approximately
0.9mlkg−1h−1in fresh water, a value that was significantly
(P<0.01) increased to 3.6mlkg−1h−1
1.5mmoll−1sodium nitroprusside added to the water (Fig. 3).
The response to sodium nitroprusside was totally abolished by
administration of 3µgg−1saralasin. Saralasin alone did not
result in alteration of drinking rate in trout fry.
by exposure to
Effects of angiotensin and saralasin on blood pressure
Hypertension in response to AngII and related peptides has
been described in a number of studies in rainbow trout and
other fish species (Platzack et al. 1993; Axelsson et al. 1994;
Olson et al. 1994; Le Mevel et al. 1994; Oudit and Butler,
1995b). The present results agree with previous in vivo work
which has focused on the hypertensive response to AngII,
occurring immediately and continuing for 20–30min post-
administration (Fig. 1; Platzack et al. 1993; Axelsson et al.
1994; Olson et al. 1994; Le Mevel et al. 1994; Oudit and
Butler, 1995b). A response not reported previously is that, after
approximately 50min, a significant hypotension develops,
lasting for at least 30min (Fig. 1). Conklin and Olson (1994b)
showed that the epibranchial artery and anterior cardinal vein
from rainbow trout responded to AngII with a transitory
contraction followed by a 5min relaxation, a similar response
but on a much shorter time scale than noted here in vivo
(Fig. 1). Relaxation of large blood vessels in response to AngII
(Conklin and Olson, 1994b) could account for the hypotension
noted here in vivo, but this point requires further study.
The hypotension observed in vivo in response to AngII was
unexpected. It could result from a direct effect of AngII, which
presumably overrides any
mechanisms. Other possibilities for this response include a
cardiovascular reflex response to the initial hypertension or that
the hypotension may arise as a consequence of release of other
vasodilators (e.g. vasodilator prostaglandins, Olson et al.
1997); however, this is an area requiring further study.
Saralasin failed to inhibit the angiotensin-dependent
hypertension in eel Anguilla rostrata, sculpin Myoxocephalus
octodecimspinosus and dogfish Squalus acanthias (Nishimura
et al. 1978; Carroll, 1981), a result confirmed in the present
study in trout (Fig. 1). However, the hypotensive effects of
AngII in rainbow trout were substantially attenuated by co-
administration with saralasin, with a return to normal blood
pressure within 20min (Fig. 1). Some possible reasons for this
response are (a) that the hypertensive and hypotensive
responses to AngII involve two populations of receptors
(Conklin and Olson, 1994a,b) with different saralasin
sensitivities, (b) that AngII metabolites, e.g. the heptapeptide
AngIII and the hexapeptide AngIV, may be involved since
these peptides elicit circulatory responses mediated by AngII
receptors in mammals (Head and Williams, 1992; Wright and
Harding, 1994) and (c) that the hypotensive effect of AngII is
indirect and mediated by other vasodilators, e.g. bradykinin
and vasodilator prostaglandins. However, further work is
required to explore these possibilities.
A doubling of pulse pressure during the 5min hypertensive
phase (Table 1; Fig. 1) could indicate decreased compliance in
the arterial system; however, normal values were rapidly
regained even during the hypotensive phase (Table 1). The
mechanisms involved are not understood and merit further
Effects of angiotensin and saralasin on heart rate
Previous studies in mammals have shown that the
chronotropic effects of AngII may be direct (Baker et al. 1992)
or caused by modification of vagal tone (Reid, 1992), but in
fish the responses of heart rate to AngII are variable. In the
Antarctic fish Pagothenia borchrevinki, heart rate decreased in
response to AngII (Axelsson et al. 1994), while it was
unchanged in cod Gadus morhua after administration of AngI
(Platzack et al. 1993). The heart rate of rainbow trout increased
following intracerebroventricular administration of AngII (Le
Mevel et al. 1994). In eels Anguilla anguilla, there was a small
J. FUENTES AND F. B. EDDY
Drinking rate (mlkg−1h−1)
Control SNPSNP+Sara Sara
Fig. 3. Drinking rates (mlkg−1h−1) in rainbow trout fry (mass 2–3g)
in response to an intramuscular injection of saline (control), an
intramuscular injection of 3µgg−1saralasin (Sara), exposure to
1.5mmoll−1sodium nitroprusside (SNP) added to the water and
exposure to 1.5mmoll−1water-borne sodium nitroprusside plus an
intramuscular injection of 3µgg−1
**Significant difference (P<0.01) from the control value (one-way
ANOVA). Results are as mean + S.E.M. of 8–10 fish (values of N are
given within bars).
AngII and cardiovascular responses in trout
but significant increase in heart rate in response to intravenous
injections of AngII, with the possible involvement of
catecholamines (Oudit and Butler, 1995a). In the present study,
AngII has a direct chronotropic effect on trout heart, since co-
administration of saralasin (an inhibitor specific to the RAS;
Moore and Fulton, 1984) significantly attenuated the response
(Fig. 2). The reason that the heart rate recorded in vivo
increased in response to AngII, whereas the perfused heart in
vitro did not (Olson et al. 1994), is unknown but could be
related to the tissue specificity of AngII cardiovascular effects,
as suggested previously (Olson et al. 1994; Conklin and Olson,
The physiological significance of the hypotensive effects of
AngII recorded here in vivo is unknown, but it may be linked
with regulation of blood pressure. Although the control of
contraction/relaxation in large vessels is thought to be of
neuronal origin, the microcirculation is believed to be a major
effector of the actions of the RAS in fish (Olson et al. 1994).
However, the presence of specific receptors for AngII in the
ventral and dorsal aortas has been demonstrated in rainbow
trout (Cobb and Brown, 1992), making them accessible targets
for changes in humoral AngII levels.
In fish, hypovolaemia and hypotension are major
determinants of the dipsogenic response (Takei, 1993), and
the involvement of the RAS in the control of drinking has
been demonstrated on many occasions. The drinking
response may be initiated either by administration of
exogenous AngI or AngII (Perrot et al. 1992; Fuentes and
Eddy, 1996) or by hypotensive agents such as papaverine
(Balment and Carrick, 1985). Similar results are obtained
using the vasodilator, sodium nitroprusside (Fuentes et al.
1996) and this response is inhibited by saralasin (Fig. 3). The
short-lived hypertensive response to AngII which has been
observed on many occasions (Platzack et al. 1993; Axelsson
et al. 1994; Olson et al. 1994; Le Mevel et al. 1994; Oudit
and Butler, 1995b; and Fig. 1) seems unlikely to be a major
stimulus for sustained drinking since, in Japanese eels
Anguilla japonica, administration of AngII resulted in
simultaneous hypertension and inhibition of drinking (Hirano
and Hasegawa, 1984).
Hypotensive agents such as papaverine induced drinking in
freshwater and seawater European eels Anguilla anguilla
(Tierney et al. 1995) by stimulating the endogenous RAS, a
response inhibited by the angiotensin-converting enzyme
inhibitor captopril. Thus, hypotension alone was insufficient to
produce the drinking response, although any hypotensive
effects of AngII in eels (Tierney et al. 1995) may have been
masked by the effects of the hypotensive agent itself. The
present study shows that AngII treatment, in the form of a
single bolus, causes a prolonged hypotension, which is in
keeping with the time course for sustained drinking (Perrot et
1992; Fuentes and Eddy, 1996). Responses to
hypovolaemia or other appropriate stimuli could involve the
release of AngII, resulting in a period of drinking that
continues until sufficient water has been absorbed to restore
normal electrolyte balance. The cycle could be repeated once
dehydration again reaches a critical level. However, how AngII
is involved in the coordination of hypotension and in the
initiation, continuation and termination of drinking remains
Juan Fuentes received postdoctoral support from the
Conselleria de Educacion e Ordenacion Universitaria, Xunta
de Galicia, Spain.
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