Antidiuretic hormone and angiotensin II plasma concentrations in febrile Pekin ducks

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Antidiuretic hormone and angiotensin II plasma concentrations in febrile Pekin ducks

David A. Gray and Shane K. Maloney

Department of Physiology, University of the Witwatersrand, Johannesburg 2193, South Africa

MS 7980 Received 6 March 1998; accepted after revision 3 June 1998.

ABSTRACT

Top
Abstract
Introduction
Methods
Results
Discussion
References

The objective of this study was to determine the changes in plasma concentrations of the hormones arginine vasotocin (AVT) and angiotensin II (AII) associated with lipopolysaccharide (LPS)-induced fever in Pekin ducks.

LPS, intravenously administered into conscious birds at doses of 1, 10 and 100 µg kg^-1, caused dose-dependent and monophasic increases in body temperature, with fever index values of 3�5, 7�0 and 10�6, respectively.

Plasma AVT concentrations also increased with the progression of the fever, with the largest elevation (from 8�4 � 1�6 to 25�2 � 3�2 pg ml^-1; means � s.e.m., n = 7) being caused by the highest dose of LPS.

Plasma AII concentrations did not significantly change from basal values (mean of 45�5 � 6�3 pg ml^-1 for all groups) during the acute phase of the fever response.

The osmotic status of the birds, as indicated by plasma osmolality and electrolyte values, did not significantly change in any of the experimental animals.

The elevation of AVT in avian fever leads to speculation about a possible antipyretic action of this hormone, which would have particular relevance to understanding the evolution of fever.

INTRODUCTION

Top
Abstract
Introduction
Methods
Results
Discussion
References

There is accumulating evidence to suggest that the mechanisms of avian fever are similar to those in mammals. For example, bacterial infection (D'Alecy & Kluger, 1975) or bacterial endotoxin administration in birds causes the development of fever (Kluger, 1979; Fraifeld et al.1995; Nomoto, 1996), which can be attenuated by a cyclooxygenase inhibitor (D'Alecy & Kluger, 1975). In addition, the avian acute-phase response to pathogens also appears to involve the sequestration of iron leading to hypoferraemia (Butler et al. 1973; Johnson et al. 1993). However, one area where information is decidedly lacking concerns endocrine changes associated with the febrile response of birds and the putative physiological roles of these hormones.

Fever in mammals is associated with changes in the circulating concentrations of a number of hormones including thyroid hormones, cortisol, atrial natriuretic peptide and arginine vasopressin (Riedel et al. 1986; Funyu et al.1995; Keil et al. 1996). Arginine vasopressin (AVP) is thought to be particularly important and is a strong candidate for having a role as an endogenous cryogen (Hellon et al. 1991; Kluger, 1991).

Arginine vasotocin (AVT), the neurohypophysial antidiuretic hormone (ADH) of avian and other non-mammalian vertebrates, is the phylogenetic ancestor of AVP (Munsick et al. 1960; Munsick, 1964) and has a well-characterized osmoregulatory role in birds (Simon-Oppermann et al. 1980; Gerstberger et al. 1985; Stallone & Braun, 1985). The observation that AVT reduces the body temperature of pigeons (John & George, 1992; Hassinen et al. 1994) suggests that ADH may have a cryogenic action in this animal group too, which would have important implications for understanding the origin and evolution of fever.

In the present study the plasma concentrations of AVT were measured in Pekin ducks during the acute phase of the fever response, induced by the intravenous injection of lipopolysaccharide (LPS). In addition, plasma angiotensin II (AII) concentrations were also monitored, in light of the observation that this hormone too can induce thermoregulatory responses in birds (Hassinen et al.1994).

METHODS

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Abstract
Introduction
Methods
Results
Discussion
References

Animals

The studies were carried out with seven adult (3 male and 4 female) Pekin ducks (Anas platyrhynchos) within a body weight range of 2�4-3�4 kg, housed in flocks at a room temperature of 22�C and with a natural day-night cycle. They were fed dry chicken food enriched with minerals and vitamins, and drank tap-water ad libitum.

Preparation of animals

On the morning of the experiment, usually at about 8.00 h, individual birds were removed from the flock, weighed and then placed in a cotton sling which prevented body rotation but allowed free movement of the neck and feet. A flexible cannula (Braunula G18, Braun, Melsungen, Germany) was inserted into one leg vein and kept patent by the continuous infusion of sterile heparinized (5 U ml^-1) isotonic saline at a rate of 0�1 ml min^-1 (Perfusor E, Braun). This cannula was used for the withdrawal of blood samples for the measurement of plasma variables and for the administration of LPS or saline.

Body temperatures were measured at 1 min intervals with 21 g thermocouples inside a length of polypropylene tubing (5 mm o.d.) inserted into the rectum. The rectal sphincter was located and the probe was inserted through the sphincter into the lower colon (rectum). The probe was secured in position by taping it to the tail feathers. Voltages from the ice-referenced (Ice-point reference chamber, model TRCIII, Omega, Stamford, CT, USA) thermocouples were measured with a data acquisition unit (model 3421, Hewlett-Packard, Palo Alto, CA, USA) interfaced with a PC. Voltages were converted into temperatures using equations for each thermocouple gained from calibration against a certified quartz thermocouple (Quat 100, Heraeus, Hanau, Germany). Resolution for this set-up was better than 0�1�C.

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Figure 1. LPS-induced changes in body temperature, AVT and AII concentrations
Body temperature (A), plasma AVT concentration (B) and plasma AII concentration (C) responses to the I.V. administration of saline ( cir ) or LPS at doses of 1 ( square ), 10 ( diam ) and 100 µg kg^-1 ( utri ) in 7 conscious Pekin ducks. For the LPS doses of 1 and 10 µg kg^-1 plasma AVT concentrations increased, in comparison with birds receiving saline, at about 12.00 h, but this difference only became significant at 16.00 h. With LPS given at the dose of 100 µg kg^-1, plasma AVT levels increased significantly above those for saline at 12.00 h and remained significantly greater than saline values for the duration of the experiment. At 16.00 h the plasma AVT levels associated with the LPS at 100 µg kg^-1 were significantly higher than those in birds given LPS doses of 1 and 10 µg kg^-1.

Experimental procedures

At about 10.00 h and following an equilibration period of at least 90 min, control blood samples (3�5 ml) were collected into polypropylene tubes containing 100 µl of an inhibitor solution (0�125 M EDTA and 0�025 M phenanthroline). After the samples had been thoroughly mixed the blood was centrifuged at 4000 g for 10 min and the plasma separated and stored for analysis. In addition a small (0�5 ml) blood sample was taken for osmolality and electrolyte measurements. The volume of each blood sample withdrawn (approximately 4�5 ml) was replaced by isotonic saline.

Immediately after the control blood samples had been taken the birds were given an I.V. injection of isotonic saline or LPS at a dose of 1, 10 or 100 µg kg^-1 in isotonic saline. Each bird received each of the four injection solutions, given in random order on separate occasions at least 2 weeks apart. Further blood samples were taken at hourly intervals for 6 h whilst body temperature was monitored continuously for the same period.

At the end of the series of experiments, the birds were killed by an overdose of sodium pentobarbitone (Eutha-Naze, Centaur Laboratories, Johannesburg, RSA) administered intravenously according to Animal Ethics Committee guidelines.

Analytical methods

Plasma concentrations of AVT and AII were measured, after acetone extraction, using specific radioimmunoassays (Gray & Simon, 1983, 1985). Plasma osmolality was measured by vapour pressure osmometry (5100C, Wescor, Logan, UT, USA) and sodium and potassium concentrations by flame photometry (Radiometer FLM3, Copenhagen, Denmark). Chloride was measured by coulombic titration (Radiometer CMT10).

Statistical analysis

Results are presented as means � S.E.M. For analysis of observed differences, data groups were subjected to two-way repeated measures ANOVA for time and dose of LPS followed by Student- Newman-Keuls multiple range tests when appropriate. The temperature responses were also analysed by calculating a fever index for each dose of LPS, which is essentially the area between the saline curve and each dose curve.

RESULTS

Top
Abstract
Introduction
Methods
Results
Discussion
References

The I.V. injection of LPS at doses of 1, 10 and 100 µg kg^-1 produced significant and dose-dependent increases in body temperature with maximum elevations of 0�54 � 0�21, 0�76 � 0�24 and 1�16 � 0�27�C (Fig. 1A), and fever index values of 3�5, 7�0 and 10�6, respectively. The rise in temperature commenced about 1 h following the LPS administration, reaching the maximum value after a further 2-3 h. Temperatures in the birds that received the LPS doses of 10 and 100 µg kg^-1 remained elevated for the duration of the experiment whilst temperatures with the lowest dose of LPS tended to return towards basal.

Plasma AVT concentrations also increased with the progression of the fever response (Fig. 1B), with the largest elevations being associated with the highest dose of LPS (dose F_3,18 = 5�74, P = 0�006; time F_6,36 = 12�43, P = 10^-⁶) and a positive correlation between plasma AVT concentration and body temperature (Fig. 2). Plasma AII concentrations, however, showed no significant changes (dose F_3,18 = 0�17, P = 0�91; time F_6,36 = 0�62, P = 0�71) during the acute phase of the fever response (Fig. 1C).

Table 1 indicates that there were no significant variations in the plasma osmolalities or electrolyte concentrations of any birds during the experiments. Similarly, none of the variables nor the fever or hormone responses demonstrated any significant difference between the male and female birds.

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Figure 2. Correlation between plasma AVT concentration and body temperature
Relationship between plasma AVT concentration and body temperature in 7 conscious Pekin ducks given intravenous saline ( cir ) or LPS at doses of 1 ( square ), 10 ( diam ) and 100 µg kg^-1 ( utri ). Each point is the mean value for the birds at each of the 7 sample times. r = 0�84, n = 28, P < 0�0001.

Table 1. Plasma variables in febrile Pekin ducks: changes in plasma osmolality, sodium and potassium concentrations in Pekin ducks injected intravenously with saline or LPS at doses of 1, 10 and 100 µg kg^-1

		Time after injection
	C	1 h	2 h	3 h	4 h	5 h	6 h
Osmolality (mosmol kg^-1)
Saline	303�4 � 4�7	306�1 � 3�9	303�4 � 23�9	301�7 � 5�8	304�3 � 4�6	304�3 � 3�9	302�7 � 4�9
1 µg kg^-1	301�4 � 5�1	303�2 � 4�1	304�9 � 3�7	303�8 � 4�2	300�9 � 3�7	303�3 � 4�6	306�4 � 5�2
10 µg kg^-1	303�7 � 3�5	301�4 � 6�1	304�3 � 2�8	305�7 � 4�3	302�2 � 6�2	302�4 � 3�5	303�9 � 2�7
100 µg kg^-1	307�2 � 4�4	300�7 � 2�8	303�6 � 3�4	302�8 � 5�4	305�2 � 6�2	303�4 � 4�4	304�6 � 2�7
[Sodium] (mmol l^-1)
Saline	149�1 � 1�8	150�7 � 1�4	150�9 � 1�9	151�4 � 2�0	151�7 � 1�8	151�5 � 1�3	151�0 � 1�1
1 µg kg^-1	150�0 � 1�0	150�0 � 1�2	152�1 � 0�8	151�0 � 1�5	150�0 � 1�4	152�0 � 1�4	151�9 � 0�9
10 µg kg^-1	148�4 � 1�0	150�4 � 0�9	147�9 � 1�4	148�6 � 1�1	148�6 � 1�2	147�9 � 1�4	149�6 � 1�3
100 µg kg^-1	150�1 � 1�3	150�6 � 1�6	149�9 � 1�4	149�9 � 1�0	150�0 � 0�9	150�9 � 0�9	149�4 � 0�8
[Potassium] (mmol l^-1)
Saline	3�24 � 0�30	3�43 � 0�15	3�37 � 0�14	3�47 � 0�20	3�36 � 0�12	3�44 � 0�10	3�33 � 0�12
1 µg kg^-1	3�68 � 0�19	3�53 � 0�08	3�51 � 0�18	3�56 � 0�08	3�43 � 0�11	3�46 � 0�09	3�36 � 0�06
10 µg kg^-1	3�34 � 0�29	3�10 � 0�14	3�34 � 0�08	3�61 � 0�12	3�60 � 0�17	3�47 � 0�09	3�50 � 0�10
100 µg kg^-1	3�36 � 0�16	3�37 � 0�12	3�49 � 0�07	3�53 � 0�09	3�44 � 0�11	3�37 � 0�08	3�39 � 0�09

C, control (i.e. before saline or LPS injection). Means � S.E.M. n = 7. There were no significant changes from control in any of the values.

DISCUSSION

Top
Abstract
Introduction
Methods
Results
Discussion
References

Although information to date about the mechanisms of, and the responses to, fever in birds is relatively scarce, it is known that exogenous pyrogen can induce a febrile response consisting of body temperature elevation (Jones et al. 1983; Nomoto, 1996) with hypoferraemia (Butler et al.1973; Johnson et al.1993) and that prostaglandins appear to be involved as mediators (D'Alecy & Kluger, 1975; Macari et al. 1993). However, no data are currently available about the possible involvement of regulatory hormones in avian fever. Therefore, the objective of this study was to determine if the acute phase response of LPS-induced fever in Pekin ducks was associated with changes in the systemic concentrations of the hormones AVT and AII. The investigation was based upon observations indicating that AVT and AII can initiate changes in body temperature in birds (John & George, 1992; Hassinen et al. 1994) and by findings in mammals which have implicated the analogous peptides in temperature regulation (Jansky, 1990; Horowitz et al. 1992).

The Pekin ducks used in the present study, like pigeons (Nomoto, 1996) and chickens (Fraifeld et al.1995), responded to intravenously injected LPS with marked and dose-dependent increases in body temperature, within 2 h of administration. The use of restraint, which may have induced a small degree of stress hyperthermia (Kluger, 1991) was obviously common to all experimental groups and does not appear to have influenced the thermoregulatory response to LPS.

As far as the hormones are concerned, there were no significant changes in the plasma concentrations of AII during the acute phase, which seems to exclude the possibility that plasma AII has a role in avian fever. It would appear that in birds, as in mammals (Jansky, 1990), any thermoregulatory action that systemic AII may have, does not apply to febrile animals. However, the possibility remains that central AII (Matsumura & Simon, 1990; Simon et al. 1992) may be physiologically important in avian fever.

Plasma AVT, on the other hand, did increase with fever and the increases were correlated with the degree of febrile response. The precise mechanism by which LPS-induced fever activates AVT secretion cannot be determined from this study; however, the fact that the osmotic status of the birds did not change suggests that osmoregulatory influences on plasma AVT, which are well known for birds (Gray & Simon, 1983; Stallone & Braun, 1986), can be ruled out. In addition, although there was a strong correlation between plasma AVT and body temperature, it is unlikely that the increased AVT in blood was caused by a direct effect of temperature, since studies in chickens (Arad & Skadhauge, 1984; Arad et al. 1985) and ducks (Hori et al. 1986; Simon & Nolte, 1990; Gray & Maloney, 1997) failed to demonstrate a hyperthermic component in the regulation of AVT secretion. It is assumed, therefore, that the elevation in circulating AVT concentrations and body temperature are two separate and direct responses to the LPS, involving independent induction mechanisms.

In mammals too, fever activates the ADH system, causing the release of AVP both centrally (Kasting et al. 1983) and peripherally (Riedel et al.1986; Keil et al.1996). However, the precise role of AVP in mammalian fever remains uncertain and although peripherally administered AVP makes rats hypothermic (Veale et al. 1981) and there is a strong negative correlation between plasma AVP and fever maximum (Kasting et al. 1981), only centrally acting ADH has been shown to have antipyretic actions (Hellon et al.1991; Kluger, 1991). In ducks, both AVT and AII have been measured in cerebrospinal fluid (CSF) with both hormones showing an independence between central and systemic regulation (Gray & Simon, 1987). Clearly, it would be extremely interesting to know whether or not central AVT and/or AII systems are activated by fever in birds and whether or not the increase in systemic AVT reflects similar central changes. However, that was not the aim of the present study.

In the absence of any information about central AVT or AII, we are left to speculate about the possible role of an elevated plasma AVT concentration in the febrile ducks. It may well be that the significance of the increased systemic AVT lies in its well-documented renal actions (Gerstberger et al.1985: Stallone & Braun, 1986). It is interesting to note that despite the marked increase in plasma AVT concentration, there was no apparent change in the osmotic status of the febrile birds. Presumably, any increase in renal water uptake was balanced by evaporative water loss. Perhaps more speculative is the idea that the elevation in circulating AVT in the ducks is linked to its known hypothermic effect in birds (John & George, 1992; Hassinen et al.1994) and that antipyresis can be added to the list of actions attributable to avian AVT. Possible mechanisms by which AVT may act as a cryogen include the inhibition of thyroid hormone secretion (John et al. 1995) and/or the reduction of metabolic rate (John & George, 1992), which have been demonstrated to be effects of AVT in birds. Alternatively, it could be that the brain-intrinsic vasotocinergic system (Berk et al. 1982; Weindl & Sofroniew, 1982; Schmid et al. 1995) is activated by circulating AVT at areas lacking a blood- brain barrier, such as the circumventricular organs (Schmid & Simon, 1996).

The implication of the present study, that the list of similarities between avian and mammalian fever can be extended to include a cryogenic action of ADH, together with other similarities with reptilian fever (Kluger, 1979, 1991) provides important information about the evolution of fever. The apparent involvement of ADH in both birds and mammals is evidence in support of the idea that the febrile mechanism has a common origin. Future experiments, which will examine the role of central AVT and AII in fever, could very well promote this concept still further.

Acknowledgements

The technical assistance of Fanny Marcos and Gail Brunton is much appreciated, as is the animal care provided by the Central Animal Unit of the University of the Witwatersrand. This study was approved by the Animal Ethics Committee of the the University of the Witwatersrand (number 96/59/3) and was supported by funding from the Foundation for Research Development (FRD) of South Africa. S. K. M. was in receipt of a University of the Witwatersrand post-doctoral fellowship.

Corresponding author

D. A. Gray: Department of Physiology, University of the Witwatersrand, Johannesburg 2193, South Africa.

Email: 057gray{at}chiron.wits.ac.za

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				C. A. Richmond Effects of Hydration on Febrile Temperature Patterns in Rabbits Biol Res Nurs, April 1, 2001; 2(4): 277 - 291. [Abstract] [PDF]

				K. C. Bicego-Nahas, A. A. Steiner, E. C. Carnio, J. Antunes-Rodrigues, and L. G. S. Branco Antipyretic effect of arginine vasotocin in toads Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2000; 278(6): R1408 - R1414. [Abstract] [Full Text] [PDF]