AJP - Regu AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 279: R1105-R1111, 2000;
0363-6119/00 $5.00
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takei, Y.
Right arrow Articles by Tsuchida, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takei, Y.
Right arrow Articles by Tsuchida, T.
Vol. 279, Issue 3, R1105-R1111, September 2000

Role of the renin-angiotensin system in drinking of seawater-adapted eels Anguilla japonica: a reevaluation

Yoshio Takei and Takamasa Tsuchida

Ocean Research Institute, The University of Tokyo, Tokyo 164-8639, Japan


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

The role of ANG II, a potent dipsogenic hormone, in copious drinking of seawater eels was examined. SQ-14225 (SQ), an angiotensin-converting enzyme inhibitor, infused intra-arterially at 0.01-1 µg · kg-1 · min-1, depressed drinking and arterial blood pressure in a dose-dependent manner. The inhibition was accompanied by a small decrease in plasma ANG II concentration, which became significant at 1 µg · kg-1 · min-1. After the infusate was changed back to the vehicle, the depression of drinking and arterial pressure continued for >2 h, although plasma ANG II concentration rebounded above the level before SQ infusion. By contrast, infusion of anti-ANG II serum (0.01-1 µg · kg-1 · min-1) did not suppress drinking and arterial pressure, although plasma ANG II concentration decreased to undetectable levels. Plasma atrial natriuretic peptide and plasma osmolality, which influence drinking rate in eels, did not change during SQ or antiserum infusions. These results suggest that the renin-angiotensin system plays only a minor role in the vigorous drinking observed in seawater eels. The results also suggest that the antidipsogenic and vasodepressor effects of SQ in seawater eels are not due solely to the inhibition of ANG II formation in plasma.

converting enzyme inhibition by SQ-14225; immunoneutralization of angiotensin II; water intake; blood pressure; atrial natriuretic peptide


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

BECAUSE ORAL INTAKE is the sole means to ingest water from the environment for seawater teleosts, they vigorously drink seawater to compensate for water lost osmotically across the body surfaces (17, 23, 25, 40). Ingested seawater is desalted and diluted to isotonicity in the anterior gut and, finally, absorbed by the posterior gut together with Na+ and Cl- (19, 24, 27). In fact, if drunk water is drained through an esophageal fistula, eels transferred to seawater suffered from gradual hypovolemia and hypernatremia and, finally, die 5 days after transfer (43). Accordingly, it is obvious that drinking is essential for teleost fish to survive in seawater.

It is generally accepted that thirst in terrestrial mammals, birds, and reptiles is induced principally by three major stimuli: an increase in plasma osmolality (cellular dehydration), a decrease in blood volume (extracellular dehydration), and an increase in plasma ANG II (11). By contrast, atrial natriuretic peptide (ANP) is recognized as a sole antidipsogenic hormone (29). In teleost fish, however, extracellular dehydration and ANG II are potent dipsogenic stimuli (7, 17, 40), but cellular dehydration caused by injections of hypertonic solutions is strongly antidipsogenic in the eel (42). Because fish drink immediately after exposure to seawater in response to Cl- in the media (17), drinking is ensured without increases in plasma osmolality. Recently, ANP was found to be a highly potent antidipsogen in the eel (46).

It is uncertain which of the dipsogenic stimuli are involved in copious drinking of seawater teleosts. Although plasma osmolality of seawater fish is generally higher than that of freshwater fish, a hyperosmotic stimulus (cellular dehydration) may play a minor role, inasmuch as it apparently inhibits drinking in the eel (42). The involvement of a hypovolemic stimulus (extracellular dehydration) is also unlikely, since blood volume does not differ between seawater- and freshwater-adapted eels (32). The most probable candidate is ANG II, because its plasma concentration or plasma renin activity is higher in seawater-adapted euryhaline fish than in freshwater fish (16, 38, 45). However, there are conflicting data showing that plasma ANG II concentration and plasma renin activity do not differ between freshwater- and seawater-adapted eels (32, 33, 39, 46), although they transiently increase after seawater transfer. Therefore, it remains undetermined whether ANG II is important for drinking of seawater fish.

Various types of angiotensin-converting enzyme (ACE) inhibitors have been widely used in mammals to evaluate the role of ANG II in hemodynamic and hydromineral regulation (10). With respect to thirst regulation, however, the effects of ACE inhibitors are biphasic, with an inhibition or stimulation depending on the dose (2). In fish, large doses of ACE inhibitors resulted in the inhibition of drinking in seawater- but not in freshwater-adapted fish (1, 14, 28, 36, 45). In goldfish, however, SQ-14225 caused dose-related inhibition or stimulation of drinking (34). Furthermore, SQ-20881 failed to inhibit drinking in some marine fish, although it was effective in inhibiting vasopressor action of ANG I (3). Therefore, the ACE inhibitors should be used with caution.

The aim of the present study is twofold. The first is to evaluate the role of the endogenous renin-angiotensin system in copious drinking of seawater eels. To this end, plasma ANG II concentration was depressed by two different mechanisms: slow infusion of an ACE inhibitor to inhibit ANG II formation and anti-ANG II serum to neutralize free ANG II in plasma. The antiserum was used instead of competitive ANG II receptor antagonists, since the latter are without effect in the eel (31). The second is to determine whether the potent antidipsogenic effect of ANP observed in seawater eels is mediated by the accompanying depression of endogenous ANG II (46), since ANG II is a potent dipsogen in eels (47). Plasma ANP concentrations, arterial pressure, and plasma osmolality were monitored throughout the infusion, since these factors are shown to affect drinking in eels (18, 42, 46).


    MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Animals. Cultured Japanese eels, Anguilla japonica, were purchased from a local dealer. They were kept in a 1-ton freshwater tank for a few days and then transferred to a 0.5-ton seawater tank and acclimated there for >2 wk before use. Seawater from the Pacific Ocean was purchased from Tokai Kisen (Tokyo, Japan). The Cl- concentration in the tank was checked regularly. Water in the tank was continuously filtered, aerated, and thermoregulated at 18 ± 0.5°C. Eels were not fed after purchase. They weighed 192.4 ± 2.9 (SE) g (n = 17) at the time of the experiment. Animal care and protocols for animal experiments were performed according to the guidelines established by the Graduate School of Science, The University of Tokyo.

Surgical procedures. Eels were anesthetized in 0.1% (wt/vol) tricaine methanesulfonate (Sigma Chemical, St. Louis, MO) in seawater neutralized with sodium bicarbonate for 10 min. Vinyl tubes (1.5 mm OD) were inserted into the esophagus and stomach, as described previously (39). The esophageal catheter was used for measurement of drinking rate and the stomach catheter for reintroduction of drunk water. In addition, polyethylene tubes (0.8 mm OD) were inserted into the dorsal aorta and ventral aorta, the former being used for drug infusion and blood pressure measurement and the latter for blood sampling. The eels that bled >0.05 ml (0.7% of total blood volume) during surgery were excluded from the experiment because of accelerated drinking rate in these fish.

After surgery the esophageal catheter was connected to a drop counter and the stomach catheter to a pulse injector synchronized with the drop counter (43). Eighty percent seawater was reintroduced into the stomach, because the seawater that appeared from the esophageal catheter was diluted to this concentration by desalting during passage through the esophagus (19, 24). The catheters in the aorta were connected to plastic syringes filled with 0.9% NaCl solution. The catheter in the dorsal aorta was connected via a three-way stopcock to a 1-ml syringe for drug infusion and to a pressure transducer (model DX-300, Nihon Kohden, Tokyo, Japan). The transducer was connected to a polygraph (366 system, NEC-San-ei, Tokyo, Japan) and a pen recorder for continuous measurement of arterial pressure. Eels were allowed to recover from anesthesia for >18 h postoperatively.

Experimental protocol. Initially, various ANG II receptor antagonists, such as saralasin, losartan (CV-11974), and CGP-42112, were tested in terms of the vasopressor effect. However, none was an effective blocker in the eel, as in other nonmammalian species (20, 30, 44), except losartan in the trout (8). Therefore, an ACE inhibitor and an anti-ANG II serum were used to block the ANG II effect. Eels were divided into two groups: one received SQ-14225 infusions (n = 8), and the other received anti-ANG II serum infusions (n = 6). The anti-ANG II serum was raised against mammalian ANG II and cross-reacted 100% with eel ANG II (46). The infusion was initiated with a vehicle (0.9% NaCl containing 0.01% Triton X-100) for 1 h and then with increasing doses of SQ-14225 (0.01, 0.1, and 1 µg · kg-1 · min-1) or antiserum (0.01, 0.1, and 1 µl · kg-1 · min-1) for 30 min at each dose and ended with a vehicle infusion for >2 h. Normal rabbit serum was also infused on the same time schedule in three different eels, which served as controls for antiserum infusion. Infusion rate was 0.3 ml/30 min, whereas 0.6 ml of blood was sampled every 30 min into the chilled syringe containing 10% 2K-EDTA (10 µl/ml blood). After centrifugation, plasma was saved while blood cells were injected into the circulation with 0.3 ml of saline in 5 min to avoid changes in blood volume. Before injection, blood cells were washed twice with 1 ml of saline to remove EDTA.

The plasma parameters measured were Na+, ANP, and ANG II concentrations and osmolality. Plasma Na+ concentration was determined with an atomic absorption spectrophotometer (model Z5300, Hitachi, Tokyo, Japan) and plasma osmolality with a vapor pressure osmometer (model 5500, Wescor). Plasma ANG II and ANP concentrations were measured by homologous RIA with 50 µl of plasma (22, 46). The intra- and interassay coefficients of variation were 5.2 and 12.6% for ANG II and 5.1 and 11.5% for ANP, respectively. After infusion of anti-ANG II serum or normal rabbit serum, protein A-Sepharose CL-4B (3 mg/100 µl; Pharmacia Biotech, Uppsala, Sweden) was added to 100 µl of plasma, and the mixture was incubated for 50 min at 4°C with gentle shaking. The incubate was then centrifuged at 24,000 g for 20 min at 4°C to remove IgG-coupled ANG II. The supernatant was lyophilized, reconstituted in 100 µl of water, and used for measurement of ANG II by RIA. All determinations were made in duplicate or triplicate.

Analysis of data. The time-course data were analyzed statistically by ANOVA followed by Tukey's test at each time point. Significance was determined at P < 0.05. Values are means ± SE.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Effects of SQ-14225 on drinking, plasma ANG II, and blood pressure. Infusion of SQ-14225 (0.01-1 µg · kg-1 · min-1) inhibited drinking in seawater eels in a dose-dependent manner (Fig. 1); the intake at 1 µg was as low as the level of freshwater fish (47). The water intake recovered after infusate was changed from SQ-14225 to saline, but it was still significantly lower than the normal intake of seawater fish even after 2 h. Plasma ANG II concentration also appeared to decrease dose dependently during SQ-14225 infusion (Fig. 1B). However, the decrease was significant only at the highest dose. Plasma ANG II concentration rebounded above the normal level for 2 h after SQ-14225 was replaced by saline, although drinking was still significantly inhibited during the period. Changes in arterial pressure were similar to changes in drinking rate: a profound decrease during SQ-14225 infusion followed by a small recovery after its termination (Fig. 1C). The hypotension continued for >2 h after termination of SQ-14225 infusion, despite an increase in plasma ANG II.


View larger version (17K):
[in this window]
[in a new window]
  		Fig. 1.   Changes in drinking rate, plasma ANG II concentration, and arterial blood pressure after infusion of SQ-14225 in seawater eels (n = 8). * P < 0.05 compared with initial vehicle infusion.

Effects of anti-ANG II serum on drinking, plasma ANG II, and blood pressure. Infusion of anti-ANG II serum (0.01-1 µl · kg-1 · min-1) caused only slight, nonsignificant decreases in drinking rate (Fig. 2A). By contrast, plasma ANG II concentration profoundly decreased during antiserum infusion, and it fell to undetectable levels (<0.3 fmol/ml) at 1 µl · kg-1 · min-1 (Fig. 2B). The low levels continued for >2 h after termination of antiserum infusion. Arterial blood pressure did not change during antiserum infusion, despite profound decreases in plasma ANG II concentration (Fig. 2C). No changes were observed in drinking rate, plasma ANG II concentration, and blood pressure during infusion of normal rabbit serum (data not shown).


View larger version (17K):
[in this window]
[in a new window]
  		Fig. 2.   Changes in drinking rate, plasma ANG II concentration, and arterial blood pressure after infusion of anti-ANG II serum in seawater eels (n = 6). Antiserum was diluted with 0.9% NaCl, and each volume was infused in 0.3 ml as indicated on the abscissa. * P < 0.05 compared with initial vehicle infusion.

Changes in plasma ANP, Na+, and osmolality. Plasma ANP concentration did not show consistent changes during infusion of SQ-14225 and anti-ANG II serum (Fig. 3, A and D). Changes in plasma Na+ concentration (Fig. 3, B and E) and plasma osmolality (Fig. 3, C and F) were also unchanged during SQ-14225 or antiserum infusion. The infusion of normal rabbit serum did not change these parameters (data not shown).


View larger version (20K):
[in this window]
[in a new window]
  		Fig. 3.   Changes in plasma atrial natriuretic peptide (ANP) concentration, plasma Na+ concentration, and plasma osmolality after infusion of SQ-14224 (n = 8) or anti-ANG II serum (n = 6) in seawater eels.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Role of ANG II in drinking of seawater fish. Teleost fishes are known to drink copiously in seawater to compensate for water lost osmotically across the body surfaces (23). Among major dipsogenic stimuli identified to date, i.e., osmotic stimulus, volemic stimulus, and ANG II (11), the osmotic stimulus may play a significant role in seawater drinking, because plasma osmolality is invariably higher in seawater fish than in freshwater fish. However, fish possess a mechanism to start drinking in response to osmolytes in external media without changes in plasma osmolality (17). Furthermore, an acute increase in plasma osmolality by bolus injections of hypertonic solutions inhibited drinking in eels (42), although the same procedure potently induces drinking in tetrapods (11, 40).

In contrast to the osmotic stimulus, the hypovolemic stimulus was potently dipsogenic in eels (17), and blood volume decreased transiently after transfer of freshwater fish to seawater (25). However, blood volume gradually returns to normal and fish become normovolemic after seawater adaptation (32). Among three major dipsogenic stimuli identified in mammals, therefore, ANG II appears to be the most probable candidate responsible for drinking of seawater-adapted fish.

It has been reported that plasma renin activity or ANG II concentration was higher in the seawater-adapted eel Anguilla anguilla than in freshwater eels (16, 45). In another eel species, A. japonica, plasma ANG II concentration increased transiently after transfer to seawater (33). However, it decreases gradually during the course of seawater adaptation, so that plasma renin activity and ANG II concentration do not differ between freshwater- and seawater-adapted eels (33, 39, 46). Although a possibility still remains that the dipsogenic receptors for ANG II are sensitized after adaptation to seawater, it is obvious that ANG II is not increased in seawater-adapted A. japonica. In the present study, drinking was not inhibited in seawater eels, even though plasma ANG II concentration was decreased to undetectable levels by infusion of anti-ANG II serum. At least in A. japonica, therefore, the role of circulating ANG II in drinking of seawater fish is not significant.

In contrast to anti-ANG II serum, inhibition of ACE by SQ-14225 profoundly inhibited drinking and lowered arterial pressure in seawater eels in this study. Similar results have previously been reported in A. anguilla (33, 45) and in other euryhaline fishes (1, 14, 28) by bolus injections of ACE inhibitors into seawater-adapted fish. These results seem to indicate that the renin-angiotensin system plays an important role in maintenance of drinking and arterial pressure in seawater fishes. However, the effect of ACE inhibitors should be interpreted with caution because of their nonspecific inhibition of other proteases (10).

Effects of SQ-14225 are not due to inhibition of ANG II formation. Although removal of plasma ANG II by anti-ANG II serum did not inhibit drinking, its slight decrease caused by SQ-14225 inhibited drinking profoundly. Furthermore, the inhibition of drinking by SQ-14225 continued after termination of infusion, even though plasma ANG II concentration rebounded above normal. Therefore, it is obvious that the antidipsogenic effect of SQ-14225 is not caused by inhibition of ANG II formation in plasma. The increase in plasma ANG II after SQ-14225 infusion may be due to the sudden conversion of accumulated ANG I to ANG II and to the activation of plasma renin activity by SQ-14225, as reported in other species (26). Changes in arterial pressure followed a time course similar to that of drinking. Therefore, the hypotension caused by SQ-14225 also is not due to the inhibition of peripheral ANG II formation. It is well known that SQ-14225 is a relatively nonspecific carboxyl dipeptidase inhibitor that blocks a variety of proteases other than ACE (4). Furthermore, ACE itself is involved in the metabolism of various biologically active peptides, including bradykinin, substance P, neurokinins, neurotensin, and opioids, some of which may affect drinking (9). Accordingly, the SQ-14225 effects cannot simply be ascribed to the inhibition of the renin-angiotensin system.

The dose of SQ-14225 used in the present study (0.01-1 µg · kg-1 · min-1) seems to be extremely low compared with those used in other fish studies. SQ-14225 inhibited drinking of seawater in A. anguilla at 72 mg/kg of intramuscular (36) or intravenous (45) injection. Similar inhibition was reported in A. japonica at 5 mg/kg of SQ-14225 (33) and in juvenile Atlantic salmon at 50 mg/kg of enalapril (14) after intraperitoneal injections. High doses of SQ-14225 were required probably because of bolus injections, since chronic oral administration of perindopril, another ACE inhibitor, at 1.4 mg · kg-1 · day-1 (~1 µg · kg-1 · min-1) suppressed plasma ANG II concentration in the rat (5).

In the goldfish, which normally drinks little, 0.1-1 mg/kg of intraperitoneal SQ-14225 stimulated drinking but 10-50 mg/kg was without effect (34). Similar dose-related effects of SQ-14225 have been reported in the rat, where low doses of SQ-14225 enhanced drinking, whereas high doses were generally inhibitory (12). It is assumed that low doses of SQ-14225 inhibit only peripheral ACE (37), and increased plasma ANG I is converted to ANG II in the brain to stimulate drinking. At high doses, however, SQ-14225 may inhibit peripheral and brain ACE to suppress drinking. In the present study, low doses of SQ-14225 inhibited drinking, but it is not known whether SQ-14225 penetrated the eel brain to inhibit brain ACE. The presence of ACE in eel brain has not been examined.

Antidipsogenic effect of ANP is not mediated by decreased plasma ANG II. ANP infusion at physiological doses inhibited drinking with a concomitant decrease in plasma ANG II concentration in seawater eels (46). Because ANG II is highly dipsogenic in the eel (47), there is a possibility that the antidipsogenic effect of ANP is mediated by suppression of plasma ANG II concentration. However, the present study showed that removal of ANG II from plasma with anti-ANG II serum did not inhibit drinking in seawater eels. Therefore, ANP may inhibit drinking directly by acting on the brain in the eel, as in the rat (29). It has been suggested that ANG II acts on the brain, probably the medulla oblongata, of eels (40, 41). Because eels are extremely sensitive to the antidipsogenic action of ANP compared with mammals (29, 46), the eel may provide a good model to pursue the site of action of ANP in the brain.

Perspectives

The present study provides evidence to suggest that plasma ANG II is not responsible for drinking of seawater in A. japonica. Because ANG II and ANP are hormones that are secreted immediately after changes in external media and quickly disappear from the circulation, they may be important only at the transition from freshwater to seawater (21, 33). A number of osmoregulatory hormones, such as cortisol, growth hormone, and prolactin (15), have slow and long-lasting action. In fact, cortisol has been shown to regulate drinking in fish (14). It is of interest to examine how ANG II and ANP affect the secretion of these long-acting hormones to regulate long-term drinking in seawater fish.

An acute increase in plasma osmolality inhibits drinking in eels probably because of profound increases in plasma ANP concentration (21, 42). Therefore, it is possible that the higher plasma osmolality of seawater-adapted eels is the cause of their continuous drinking, since their plasma ANP level does not differ from that of freshwater eels (22). It is reported that slow infusion of hypertonic saline increased drinking rate in freshwater eels (17).

It is evident that inhibition of drinking by SQ-14225 is not due to inhibition of the peripheral renin-angiotensin system. However, there is a possibility that SQ-14225 inhibits brain ACE to inhibit local ANG II formation, although there is no evidence for the presence of a brain renin-angiotensin system in the eel. Furthermore, if ANG II acts on the circumventricular structures that lack a blood-brain barrier in the eel, as in mammals and birds (11), even anti-ANG II serum with high molecular mass may block the ANG II effect in the brain. Therefore, it is important to determine the site of action of ANG II and the presence of an intrinsic renin-angiotensin system in the eel brain to pursue this issue.

Finally, what is the cause of profound inhibition of drinking after SQ-14225 infusion? In addition to conversion of ANG I to ANG II, ACE is importantly involved in degradation of bradykinin to inactive metabolites, which gives rise to the name kininase II. Therefore, it is possible that the antidipsogenic and vasodepressor effects of SQ-14225 are mediated by activation of the kallikrein-kinin system. Bradykinin is vasodepressor (6) and dipsogenic (13) in mammals. However, bradykinin causes a triphasic effect on blood pressure in the trout (35). Very recently, we found that an infusion of eel bradykinin into seawater eels potently inhibited drinking (unpublished data). Thus bradykinin could be a mediator of the antidipsogenic action of SQ-14225 in seawater eels.


    ACKNOWLEDGEMENTS

The authors gratefully acknowledge the excellent technical assistance of Sanae Hasegawa. The authors are grateful to Dr. Ken'ichi Yamaguchi (Dept. of Physiology, Niigata University School of Medicine) for the generous gift of ANG II antisera and to Sankyo Pharmaceutical for providing SQ-14225 (captopril).


    FOOTNOTES

This investigation was supported by Ministry of Education, Science, and Culture of Japan Grant 09102008.

Address for reprint requests and other correspondence: Y. Takei, Laboratory of Physiology, Ocean Research Institute, The University of Tokyo, 1-15-1 Minamidai, Nakano, 164-8639 Tokyo, Japan (E-mail: takei{at}ori.u-tokyo.ac.jp).

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.

Received 22 December 1999; accepted in final form 24 April 2000.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

1.   Balment, RJ, and Carrick S. Endogenous renin-angiotensin system and drinking behavior in flounder. Am J Physiol Regulatory Integrative Comp Physiol 248: R157-R160, 1985.

2.   Barney, CC, Threatte RM, and Fregly MJ. Water deprivation-induced drinking in rats: role of angiotensin II. Am J Physiol Regulatory Integrative Comp Physiol 244: R244-R248, 1983.

3.   Beasley, D, Shier DN, Malvin RL, and Smith G. Angiotensin-stimulated drinking in marine fish. Am J Physiol Regulatory Integrative Comp Physiol 250: R1034-R1038, 1986.

4.   Bennett, T, and Gardiner SM. Differential effects of various angiotensin-converting enzyme inhibitors. In: The Renin-Angiotensin System, edited by Robertson JIS, and Nicolls MG.. London: Gower, 1993, p. 98.1-98.16.

5.   Campbell, DJ, Kladis A, and Duncan A-M. Effects of converting enzyme inhibitors on angiotensin and bradykinin peptides. Hypertension 23: 439-449, 1994[Abstract/Free Full Text].

6.   Carretero, OA, Miyazaki S, and Scicli AG. Role of kinins in the acute antihypertensive effect of the converting enzyme inhibitor, captopril. Hypertension 3: 18-22, 1981[Abstract/Free Full Text].

7.   Carrick, S, and Balment RJ. The renin-angiotensin system and drinking in the euryhaline flounder, Plachthyes flesus. Gen Comp Endocrinol 51: 423-443, 1983[ISI][Medline].

8.   Cobb, CS, Williamson R, and Brown JA. Angiotensin II-induced calcium signaling in isolated glomeruli from fish kidney (Oncorhynchus mykiss) and effects of losartan. Gen Comp Endocrinol 113: 312-321, 1999[ISI][Medline].

9.   Ehlers, MRW, and Riordan JF. Angiotensin converting enzyme: biochemistry and molecular biology. In: Hypertension: Pathophysiology, Diagnosis, and Management, edited by Laragh JH, and Brenner BM.. New York: Raven, 1990, p. 1217-1231.

10.   Ferguson, RK, and Vlasses PH. Angiotensin-converting enzyme inhibitors: an overview. In: Angiotensin-Converting Enzyme Inhibitors, edited by Ferguson RK, and Vlasses PH.. New York: Futura, 1987, p. 1-28.

11.   Fitzsimons, JT. Angiotensin, thirst, and sodium appetite. Physiol Rev 78: 583-686, 1998[Abstract/Free Full Text].

12.   Fitzsimons, JT, and Elfont RM. Angiotensin does contribute to drinking induced by caval ligation in the rat. Am J Physiol Regulatory Integrative Comp Physiol 243: R558-R562, 1982.

13.   Fregly, MJ, and Rowland NE. Bradykinin-induced dipsogenesis in captopril-treated rats. Brain Res Bull 26: 169-172, 1991[ISI][Medline].

14.   Fuentes, J, and Eddy FB. Effect of manipulation of the renin-angiotensin system in control of drinking in juvenile Atlantic salmon (Salmo salar L) in fresh water and after transfer to sea water. J Comp Physiol [B] 167: 438-443, 1997[Medline].

15.   Hazon, N, and Balment RJ. Endocrinology. In: The Physiology of Fishes (2nd ed.), edited by Evans DH.. Boca Raton, FL: CRC, 1998, p. 441-464.

16.   Henderson, IW, Jotisankasa V, Mosley W, and Oguri M. Endocrine and environmental influences upon plasma cortisol concentrations and plasma renin activity of the eel, Anguilla anguilla L. J Endocrinol 70: 81-95, 1976[Abstract].

17.   Hirano, T. Some factors regulating water intake by the eel, Anguilla japonica. J Exp Biol 61: 737-747, 1974[Abstract/Free Full Text].

18.   Hirano, T, and Hasegawa S. Effects of angiotensin II and other vasoactive substances on drinking in the eel, Anguilla japonica. Zool Sci 1: 106-113, 1983.

19.   Hirano, T, Morisawa M, Ando M, and Utida S. Adaptive changes in ion and water transport mechanism in the eel intestine. In: Intestinal Ion Transport, edited by Robinson JWL. Lancaster, PA: MTP, 1976, p. 301-317.

20.   Ji, H, Sandberg K, Zhang Y, and Catt KJ. Molecular cloning, sequencing and functional expression of an amphibian angiotensin II receptor. Biochem Biophys Res Commun 194: 756-762, 1993[ISI][Medline].

21.   Kaiya, H, and Takei Y. Osmotic and volaemic regulation of atrial and ventricular natriuretic peptide secretion in conscious eels. J Endocrinol 149: 441-447, 1996[Abstract].

22.   Kaiya, H, and Takei Y. Atrial and ventricular natriuretic peptide concentrations in plasma of freshwater- and seawater-adapted eels. Gen Comp Endocrinol 102: 183-190, 1996[ISI][Medline].

23.   Karnaky, KJ, Jr. Osmotic and ionic regulation. In: The Physiology of Fishes (2nd ed.), edited by Evans DH.. Boca Raton, FL: CRC, 1998, p. 159-178.

24.   Kirsch, R, Humbert W, and Rodeau JL. Control of the blood osmolarity in fishes with references to the functional anatomy of the gut. In: Osmoregulation in Estuarine and Marine Animals, edited by Pequeux A, Gilles R, and Bolis L.. Berlin: Springer-Verlag, 1983, p. 67-92.

25.   Kirsch, R, and Mayer-Gostan N. Kinetics of water and chloride exchange during adaptation of the European eel to sea water. J Exp Biol 58: 105-121, 1973[Abstract/Free Full Text].

26.   Kobayashi, H, and Takei Y. The Renin-Angiotensin System---Comparative Aspects. Berlin: Springer, 1996, p. 108-111, 115-154.

27.   Loretz, CA. Electrophysiology of ion transport in teleost intestinal cells. In: Cellular and Molecular Approaches to Fish Ionic Regulation, edited by Wood CM, and Shuttleworth TJ.. San Diego, CA: Academic, 1995, p. 25-56.

28.   Malvin, RL, Schiff D, and Eiger S. Angiotensin and drinking rates in the euryhaline killifish. Am J Physiol Regulatory Integrative Comp Physiol 239: R31-R34, 1980.

29.   McCann, SM, Franci C, Gutkowska J, Fevaretto AL, and Antunes-Rodrigues J. Neural control of atrial natriuretic peptide actions on fluid intake and excretion. Proc Soc Exp Biol Med 213: 117-127, 1996[Medline].

30.   Murphy, TJ, Nakamura Y, Takeuchi K, and Alexander RW. A cloned angiotensin receptor isoform from the turkey adrenal gland is pharmacologically distinct from mammalian angiotensin receptors. Mol Pharmacol 44: 1-7, 1993[Abstract].

31.   Nishimura, H, Norton VM, and Bumpus FM. Lack of specific inhibition of angiotensin II in eels by angiotensin antagonists. Am J Physiol Heart Circ Physiol 235: H95-H103, 1978.

32.   Nishimura, H, Sawyer WH, and Nigrelli RF. Renin, cortisol and plasma volume in marine teleost fishes adapted to dilute media. J Endocrinol 70: 47-59, 1976[Abstract].

33.   Okawara, Y, Karakida T, Aihara M, Yamaguchi K, and Kobayashi H. Involvement of angiotensin II in water intake in the Japanese eel, Anguilla japonica. Zool Sci 4: 523-528, 1987.

34.   Okawara, Y, and Kobayashi H. Enhancement of water intake by captopril (SQ14225), an angiotensin I-converting enzyme inhibitor, in the goldfish, Carassius auratus. Gen Comp Endocrinol 69: 114-118, 1988[ISI][Medline].

35.   Olson, KR, Conklin DJ, Weaver L, Jr, Duff DW, Herman CA, Wang X, and Conlon JM. Cardiovascular effects of homologous bradykinin in rainbow trout. Am J Physiol Regulatory Integrative Comp Physiol 272: R1112-R1120, 1997[Abstract/Free Full Text].

36.   Perrott, MN, Grierson CE, Hazon N, and Balment RJ. Drinking behaviour in sea water and fresh water teleosts, the role of the renin-angiotensin system. Fish Physiol Biochem 10: 161-168, 1992.

37.   Phillips, MI, Speakman EA, and Kimura B. Tissue renin-angiotensin system. In: Cellular and Molecular Biology of the Renin-Angiotensin System, edited by Raizada MK, Phillips MI, and Summers C.. Boca Raton, FL: CRC, 1993, p. 97-130.

38.   Smith, NF, Eddy FB, Struthers AD, and Talbot C. Renin, atrial natriuretic peptide and blood plasma ions in parr and smolts of Atlantic salmon Salmo salar L. and rainbow trout Oncorhynchus mykiss (Walbaim) in fresh water and after short-term exposure to sea water. J Exp Biol 157: 63-74, 1991[Abstract/Free Full Text].

39.   Sokabe, H, Oide H, Ogawa M, and Utida S. Plasma renin activity in Japanese eels (Anguilla japonica) adapted to seawater or dehydration. Gen Comp Endocrinol 21: 160-167, 1973[ISI][Medline].

40.   Takei, Y. Comparative physiology of body fluid regulation in vertebrates with special reference to thirst regulation. Jpn J Physiol. 50: 171-186, 2000[ISI][Medline].

41.   Takei, Y, Kobayashi H, and Hirano T. Angiotensin and water intake in the Japanese eel, Anguilla japonica. Gen Comp Endocrinol 38: 466-475, 1979[ISI][Medline].

42.   Takei, Y, Okubo J, and Yamaguchi K. Effects of cellular dehydration on drinking and plasma angiotensin II level in the eel, Anguilla japonica. Zool Sci 5: 43-51, 1988.

43.   Takei, Y, Tsuchida T, and Tanakadate A. Evaluation of water intake in seawater adaptation in eels using a synchronized drop counter and pulse injector system. Zool Sci 15: 677-682, 1998.

44.   Tierney, M, Takei Y, and Hazon N. The presence of angiotensin receptors in elasmobranchs. Gen Comp Endocrinol 105: 9-17, 1997[ISI][Medline].

45.   Tierney, ML, Luke G, Cramb G, and Hazon N. The role of the renin-angiotensin system in the control of blood pressure and drinking in the European eel, Anguilla anguilla. Gen Comp Endocrinol 100: 39-48, 1995[ISI][Medline].

46.   Tsuchida, T, and Takei Y. Effects of homologous atrial natriuretic peptide on drinking and plasma ANG II level in eels. Am J Physiol Regulatory Integrative Comp Physiol 275: R1605-R1610, 1998[Abstract/Free Full Text].

47.   Tsuchida, T, and Takei Y. A potent dipsogenic action of homologous angiotensin II infused at physiological doses in eels. Zool Sci 16: 476-483, 1999.

Am J Physiol Regul Integr Comp Physiol 279(3):R1105-R1111
0363-6119/00 $5.00 Copyright © 2000 the American Physiological Society


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
O. Skott
Renin
Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2002; 282(4): R937 - R939.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
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]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takei, Y.
Right arrow Articles by Tsuchida, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takei, Y.
Right arrow Articles by Tsuchida, T.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online