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Ocean Research Institute, The University of Tokyo, Minamidai, Nakano, Tokyo 164, Japan
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ABSTRACT |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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The
effects of eel atrial natriuretic peptide (ANP) on drinking were
investigated in eels adapted to freshwater (FW) or seawater (SW) or in
FW eels whose drinking was stimulated by a 2-ml hemorrhage. An
intra-arterial infusion of ANP (0.3-3.0
pmol · kg
1 · min1), which increased
plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently
in all groups of eels. The drinking rate recovered to the level before
ANP infusion within 2 h after infusate was replaced by saline. The
inhibition at 3.0 pmol · kg1 · min1
was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II
concentration also decreased dose dependently during ANP infusion and
recovered to the initial level after saline infusion in all groups of
eels. The decrease at 3.0 pmol · kg1 · min1
was large in FW eels and hemorrhaged FW eels compared with that of SW
eels. Thus the changes in drinking rate and plasma ANG II level were
parallel during ANP infusion. Plasma sodium concentration and
osmolality decreased during ANP infusion in SW and FW eels, and they
were restored after saline infusion. In hemorrhaged FW eels, however,
ANP infusion did not alter plasma sodium concentration and osmolality.
Hematocrit did not change during ANP infusion in any group of eels.
Collectively, ANP infusion at physiological doses decreased drinking
rate and plasma ANG II concentration in parallel in both FW and SW
eels. It remains undetermined whether the inhibition of drinking is
caused by direct action of ANP or through inhibition of ANG II, which
is known as a potent dipsogen in all vertebrate species, including
eels.
water intake; Anguilla japonica
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INTRODUCTION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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THE REGULATION OF DRINKING is one of the essential osmoregulatory processes for euryhaline teleosts such as eels, which migrate between freshwater (FW) and seawater (SW) (6). In FW, they are continually faced with the need to dispose of water that enters through the body surface, and so they usually drink little water. In SW, however, they drink copious amounts of water to compensate for the loss from the body surface due to the high environmental osmotic pressure (11, 13, 25). Thus the regulation of drinking is a key process that enables euryhaline fish to survive in both FW and SW.
Atrial natriuretic peptide (ANP) is a cardiac hormone known to be involved in volume and pressure homeostasis (3, 33). In mammals, ANP is secreted in response to an increase in blood volume and it acts to decrease blood volume to normal, suggesting that ANP is a volume-regulating hormone (28). In eels, however, ANP secretion is stimulated by an increase in plasma osmolality and ANP acts to excrete sodium ions specifically, thereby promoting SW adaptation (16, 36). Concerning the intake, ANP inhibits thirst and sodium appetite in mammals (2, 41). In fish, ANP and ventricular natriuretic peptide inhibit drinking in FW eels when injected at doses that are mildly hypotensive (34). Although ANP is an SW-adapting hormone in eels (33), its effect on drinking has not been examined in SW fish.
In contrast to ANP, ANG II is a potent dipsogen in all vertebrate species examined thus far (14, 21, 22). Interaction of ANP and ANG II occurs in regulation of thirst and sodium appetite in mammals (43), as observed in regulation of aldosterone secretion (23). ANG II is a potent dipsogen also in the eel (35), but the interaction with ANP has not been examined yet.
In the present study, the effect of eel ANP on drinking was examined in both FW and SW eels by slow infusion of the hormone at doses that were shown to be nondepressor in our previous study (36). Changes in plasma ANG II concentration were measured during ANP infusion to assess the interaction of ANP and ANG II in the regulation of drinking. Because drinking is vulnerable to changes in blood volume in eels (11), the change was minimized by adjusting the volume of infusion and blood sampling. The changes in plasma sodium concentration and osmolality were also examined, because these are important regulators of drinking, especially in terrestrial animals (7).
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MATERIALS AND METHODS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Animals. Cultured Japanese eels, Anguilla japonica, were purchased from a local dealer. They were kept in a 1-ton FW tank for >1 wk before use (FW-adapted eels). Some eels were transferred to a 0.5-ton SW tank and acclimated there for >2 wk before use (SW-adapted eels). Water in the tank was continuously filtered, aerated, and thermoregulated at 18 ± 0.5°C. Eels were not fed after purchase. They weighed 181.5 ± 2.8 g (mean ± SE, n = 24) at the time of experiment.
Surgical procedures. Eels were anesthetized in 0.1% (wt/vol) tricaine methanesulfonate (Sigma, St. Louis, MO) neutralized with sodium bicarbonate for 10 min. Then vinyl tubes (1.5 mm OD) were inserted into the esophagus and stomach of eels as described previously (39). The esophageal catheter was used for measurements of drinking rate, and the stomach catheter was used for reintroduction of drunk water. In addition, polyethylene tubes (0.8 mm OD) were inserted into the dorsal and ventral aorta for infusion of drugs and blood collection, respectively. The eels that bled >0.05 ml (0.7% of blood volume) during surgery were excluded from the experiment.
After surgery, eels were transferred to a plastic trough through which aerated and thermoregulated (18°C) water constantly circulated (Fig. 1). The catheter placed in the esophagus was connected to a drop counter for continuous measurement of drinking rate. The drunk water that dropped from the esophageal catheter (0.03 ml/drop) was reintroduced into the stomach with FW (for FW-adapted fish) or 80% SW (for SW-adapted fish) by means of a pulse injector synchronized with the drop counter (39). Eighty-percent SW was used for SW fish because drunk SW that dropped from the esophageal catheter was diluted to 78.7 ± 0.02% (n = 4) because of desalting by the esophagus (13). The catheters in the aortas were connected to plastic syringes filled with 0.9% NaCl solution. The syringe connected to the dorsal aorta was set in the infusion pump for ANP infusion (Fig. 1). Eels were allowed to recover for >18 h postoperatively.
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Experimental protocol.
Three groups of eels were used in this experiment:
1) FW-adapted eels,
2) FW eels subjected to 2 ml of
hemorrhage (28.6% blood volume) on the previous day, and
3) SW-adapted eels. The second group
was prepared because drinking rate of FW eels was too low to
demonstrate clear inhibition, and because hypovolemia is a potent
stimulus for drinking in the eel (11). The eels received hourly infusions of isotonic saline followed by increasing doses of eel
ANP (Peptide Institute, Osaka, Japan) at 0.3, 1.0, and 3.0 pmol · kg1 · min1
and ended with saline infusion for 2 h. Infusion rate was 0.3 ml/h,
whereas 0.6 ml of blood was sampled every hour from the ventral aorta
into the chilled plastic syringe containing 10% 2K-EDTA
(10 µl/ml blood). Fifty microliters of collected blood were
transferred into a capillary for measurements of hematocrit and plasma
sodium concentration and osmolality. After centrifugation of the blood
sample, plasma was used for measurements of eel ANP and ANG II by
radioimmunoassay. The blood cells were washed two times with 1 ml 0.9%
saline, reconstituted with 0.3 ml of saline, and injected into the
circulation within 5 min after blood sampling. Each drop from the
esophageal catheter was monitored as a spike in the recorder, and water
intake every 10 min was stored in the memory of the drop counter (Fig.
1). The details of the drop counter and pulse injector system have been
described elsewhere (39).
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Analysis of data. Student's t-test was applied for comparison of different groups of eels. A paired t-test or Fisher's exact probability test was used for analysis of time course data. Significance was set at P < 0.05. All results are expressed as means ± SE.
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RESULTS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Plasma ANP concentration. Plasma ANP concentration increased dose dependently during ANP infusion in all groups of eels (Table 1). After infusate was changed back to saline, plasma ANP level was still high for 1 h but fell to the initial level in 2 h.
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Changes in drinking rate.
Drinking rate was very low in FW eels; however, ANP infusion decreased
it to zero (Fig.
3A). The
drinking rate recovered gradually during saline infusion, and it
rebounded above the initial level after 2 h. The dose-dependent
inhibition was more apparent in hemorrhaged FW eels, which exhibited
greater initial drinking, and eels drank practically no water at 3.0 pmol · kg1 · min1
(Fig. 3B). ANP also inhibited
copious drinking of SW eels in a dose-dependent manner (Fig.
3C). However, the inhibition was small, so that SW eels drank more water than FW eels and hemorrhaged FW
eels at 3.0 pmol · kg1 · min1.
The inhibition disappeared after saline infusion also in SW eels.
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Changes in plasma ANG II level. Plasma ANG II concentration decreased dose dependently during ANP infusion, and it was restored to the initial level after infusate was replaced by saline in all groups of eels (Fig. 4). However, the percentage of decrease was much smaller in SW eels compared with that of FW eels and hemorrhaged FW eels.
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Plasma sodium concentration, osmolality, and hematocrit. Plasma sodium concentration and osmolality were higher in SW eels than in FW eels and hemorrhaged FW eels (Fig. 5). Plasma sodium concentration and osmolality decreased dose dependently in both FW and SW eels during the ANP infusion, and the levels were restored gradually after saline infusion. However, there were no changes in plasma sodium concentration and osmolality in hemorrhaged FW eels. Hematocrit did not change during ANP infusion in all groups.
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DISCUSSION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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The present study showed that eel ANP potently inhibits water intake
and plasma ANG II concentration in a dose-dependent manner in both FW
and SW eels. The plasma ANP concentration produced by infusion of 0.3 or 1.0 pmol · kg1 · min1
was within the upper limit of individual and seasonal variation of
intact fishes (16). The ANP level after infusion of 3.0 pmol · kg1 · min1 was high, but it was
also observed endogenously after injection of hypertonic saline into FW
eels (18). Therefore, eels are highly sensitive to ANP for inhibition
of drinking and renin secretion. We reported previously that infusion
of ANP even at 3.0 pmol · kg1 · min1 did not change
arterial blood pressure in both FW and SW eels (36). Therefore, the
effects on drinking and renin secretion are more sensitive to ANP than
is the vascular effect in the eel. Furthermore, because
blood pressure and blood volume, which profoundly influence drinking
and renin secretion (11, 12, 26), were maintained constant in this
study, the ANP effects may be caused by its direct action.
In mammals, ANP has been shown to inhibit drinking and sodium appetite when administered into the cerebral ventricles (2, 41). However, the inhibition was observed only in animals whose appetite was stimulated by dehydration or ANG II injection. In contrast, the inhibition was observed even in intact eels in the present study. These results support the notion that eels are highly sensitive to the antidipsogenic effect of ANP. Furthermore, the antidipsogenic effect of ANP is more potent than the dipsogenic effect of ANG II in the eel (33), although the reverse is true in mammals (43).
Cellular dehydration, extracellular dehydration, and ANG II are major dipsogenic stimuli in birds and mammals (7, 20, 37). Hypovolemia and ANG II also stimulate drinking in the eel (11), but cellular dehydration caused by injection of hypertonic saline suppresses drinking in both FW and SW eels despite a concomitant increase in plasma ANG II level (38). Because ANP is a powerful antidipsogen in the eel, as shown in this study, and because hypernatremia profoundly augments ANP secretion in the eel (18), the unexpected inhibition of drinking after injection of hypertonic saline in the eel may be due to increased plasma ANP. An unexpected hypotension observed after injection of hypertonic saline in the eel may also be due to increased plasma ANP (30).
ANP is secreted in response to an increase in blood volume, and the increased ANP decreases blood volume by inhibiting the intake and stimulating the excretion of water and sodium (3, 28). In contrast, renin is released in response to hypovolemia and ANG II stimulates the intake and inhibits the excretion of water and sodium (20). Therefore, the renin-angiotensin system antagonizes the natriuretic peptide system in every aspect of osmoregulation. ANP inhibits renin secretion both in vivo and in vitro in selected species of mammals (4, 10), but the effect is still controversial, especially in vivo, because it decreases blood pressure (19, 29). In the present study, low doses of ANP decreased plasma ANG II concentration in vivo without changing blood pressure and blood volume. In the eel, therefore, ANP appears to be highly potent for inhibiting renin secretion by direct actions.
The present study showed that the inhibition of drinking by ANP is accompanied by a parallel decrease in plasma ANG II concentration in both FW and SW eels. Furthermore, the percentage inhibition of drinking and plasma ANG II level was similar in both FW and SW eels. Therefore, it is possible that the inhibition of drinking by ANP is mediated by a decrease in plasma ANG II. In fact, ANG II is a potent dipsogen in the eel (35) and other vertebrate species (21, 22). However, the interaction of ANP and ANG II in regulation of drinking in the eel remains to be determined.
Plasma sodium concentration and osmolality decreased in FW and SW eels but not in hemorrhaged FW eels during ANP infusion. In hemorrhaged eels, sodium-retaining mechanisms may have been maximally activated. This result, together with those reported previously (5, 34), indicates that ANP is a sodium-extruding hormone that promotes SW adaptation. In SW, however, fish have to drink SW and absorb water by the gut to cope with dehydration (6), but ANP inhibits drinking and subsequent intestinal absorption of water in SW eels (1, 24). After transfer of eels to SW, reflex drinking occurs immediately in response to chloride ions in SW (11) but the drinking rate decreases transiently for 1-2 h and increases again gradually thereafter (38). The plasma ANP level increases for 1-2 h after exposure to SW and gradually decreases to the FW level (17). Therefore, plasma ANP level does not differ between FW and SW eels, as shown in this study. Comparing the changes in drinking rate and plasma ANP level, it seems that ANP is involved in the temporary inhibition of drinking for 1-2 h after exposure to SW. Because active desalting of drunk SW occurs by the esophagus, the eels most likely suffer from severe hypernatremia if the initial burst of drinking continues after SW exposure. It seems, therefore, that the transient depression of drinking for 1-2 h after SW exposure may be beneficial to counteract the excess hypernatremia during the initial phase of SW adaptation.
Perspectives
The present study shows that ANP decreases drinking rate and plasma ANG II level (probably renin secretion) in the eel at doses that do not affect blood pressure. This is rather surprising because, in mammals, vascular effect usually overrides the other effects and ANP knockout mice exhibit normal drinking and plasma ANG II but lower blood pressure compared with normal mice (15). Therefore, the eel may serve as a good model to analyze how ANP is involved in the mechanisms regulating drinking and renin secretion.Another important aspect for future studies is whether ANP acts directly on the brain to inhibit drinking or the inhibition is mediated by depressed plasma ANG II. ANP is known to act on the brain to inhibit drinking in mammals (2, 43), but aquatic fish can stop and start drinking only by constriction and relaxation of the esophageal sphincter. Because direct application of ANG II into the cerebral ventricles of eels shows its action on the brain (31), a similar technique can be used for ANP to clarify its site of action. The mediation of ANG II in ANP action can be examined by infusing ANP with ANG II to maintain normal plasma ANG II level during ANP infusion or by using various inhibitors of the renin-angiotensin system. In A. anguilla, a bolus injection of ANG I-converting enzyme inhibitor depresses drinking in SW fish but not in FW fish (40). Thus ANG II does not seem to be involved in normal drinking in FW eels.
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ACKNOWLEDGEMENTS |
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We are grateful to Dr. H. Nishimura of the University of Tennessee, Memphis, for critical reading of this manuscript and to Dr. K. Yamaguchi of Niigata University for supplying us with ANG II antiserum.
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FOOTNOTES |
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This investigation was supported in part by a grant from the Ministry of Education, Science and Culture, Japan (09102008) to Y. Takei.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: T. Tsuchida, Laboratory of Physiology, Ocean Research Institute, The Univ. of Tokyo, 1-15-1 Minamidai, Nakano, Tokyo 164-8639, Japan.
Received 9 March 1998; accepted in final form 28 July 1998.
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Abstract
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Discussion
References
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 W. G. Anderson, Y. Takei, and N. Hazon Osmotic and volaemic effects on drinking rate in elasmobranch fish J. Exp. Biol., April 15, 2002; 205(8): 1115 - 1122. [Abstract] [Full Text] [PDF]
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Y. Takei and S. Hirose The natriuretic peptide system in eels: a key endocrine system for euryhalinity? Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2002; 282(4): R940 - R951. [Abstract] [Full Text] [PDF]
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Y. Takei, T. Tsuchida, Z. Li, and J. M. Conlon Antidipsogenic effects of eel bradykinins in the eel Anguilla japonica Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2001; 281(4): R1090 - R1096. [Abstract] [Full Text] [PDF]
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Y. Takei and T. Tsuchida Role of the renin-angiotensin system in drinking of seawater-adapted eels Anguilla japonica: a reevaluation Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2000; 279(3): R1105 - R1111. [Abstract] [Full Text] [PDF]
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) using 125I-labeled
eel ANG II. Displacement curve of human
[Asp1,Ile5]
ANG II (
), against which antiserum was originally raised, was also
given. Serial dilution curve of eel plasma (
) was parallel with
standard curve of eel ANG II.
), and SW eels (
). Data are
shown as means ± SE.
* P < 0.05 from initial value
by paired t-test.