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ANIMAL GROWTH, PHYSIOLOGY, AND REPRODUCTION |
,2
* Australian Institute of Tropical Veterinary and Animal Science and
and
Department of Physiology and Pharmacology, School of Biomedical Sciences, James Cook University, Townsville 4811, Australia
Abstract
This study investigated the effects of excess cortisol on physiological mechanisms that resist dehydration in Bos indicus steers (n = 31, 2 yr of age, 193 ± 21.47 kg mean BW) during a 90-h period. Steers were assigned randomly to one of four groups: 1) no water/no cortisol (n = 8), 2) water/no cortisol (n = 8), 3) no water/cortisol (n = 8), and 4) water/cortisol (n = 7). Animals allocated to cortisol treatment groups were given 0.1 mg•kg BW-1•h-1 of hydrocortisone suspended in isotonic saline for the duration of the study. Total body water, osmolality, hematocrit, urine output, feed and water intake, and plasma concentrations of arginine vasopressin (AVP), angiotensin II (AII), electrolytes, total protein, and albumin were determined at 24-h intervals for 90 h. In the presence of excess plasma cortisol, total body water was maintained in the presence of a water deprivation insult for 90 h, whereas hydration indices, such as total plasma protein and albumin, did not change, supporting the body water data. However, plasma osmolality increased for the water-deprived groups from 24 h (P = 0.008). Hematocrit did not reflect dehydration in any group. Water deprivation induced an increase in endogenous plasma cortisol concentrations after 60 h of the study (P = 0.028). Plasma concentrations of AVP increased with water deprivation (P = 0.006). Excess cortisol decreased the plasma concentration of AVP at 72 h only (P = 0.027) and suppressed plasma concentrations of AII at 24 and 72 h (P < 0.001 and P = 0.036, respectively). Animals treated with excess cortisol maintained urinary output for 48 h before decreasing at 72 h (P = 0.057), although there was no effect on water or feed intake. Water deprivation increased plasma sodium concentrations (P < 0.05) until 72 h, whereas potassium decreased under the influence of excess plasma cortisol (P = 0.001) at 24 h. Water deprivation increased plasma chloride concentration at 72 and 90 h (P = 0.051 and P = 0.026, respectively). Plasma phosphorus decreased at 24 h (P = 0.001) and remained at lesser concentrations for the duration of the study (P = 0.05). These results highlight the complexity of endocrine interactions associated with water balance in Bos indicus steers. We accept our hypothesis that, in the presence of excess cortisol, the renin-angiotensin-aldosterone axis is suppressed; however, homeostasis is achieved through other physiological systems.
Key Words: Angiotensin • Arginine Vasopressin • Bos indicus • Dehydration • Hydrocortisone
Introduction
Ruminants exposed to the stressors of transport and handling respond with an activation of the sympathetic-adrenal-medullary (SAM) axis and the hypothalamo-pituitary-adrenal (HPA) axis (Schaefer et al., 2001
). Because activation of the SAM axis provides for a short-term response, models that mimic the effects of the HPA axis have been favored to investigate the longer-term effects of a stressor on the physiology of an animal. The HPA axis—when activated by a stressor, such as transport and handling—produces the release of glucocorticoids and other hormones that have pathophysiological effects on an animal’s body.
We previously adapted a stress model based on cortisol infusions from Macfarlane et al. (2000) to investigate the effects of excess cortisol infusions on water balance in the Merino sheep (Parker et al., 2003). As a consequence of this previous research, it appeared that the stress hormone, cortisol, had the capacity to interfere with a principal mechanism of resistance to dehydration. Cortisol has been implicated in inhibiting the effects of arginine vasopressin (AVP) in dogs (Baas et al., 1984), and evidence indicates that elevated adrenocorticotropin hormone (ACTH) and glucocorticoids also inhibit the renin-angiotensin-aldosterone (RAA) axis (Coghlan et al., 1979). Our working hypothesis was that excess plasma concentrations of cortisol would interfere with the principal mechanisms of resistance to dehydration in Bos indicus genotypes, in particular the AVP-thirst mechanism and the RAA mechanism.
Materials and Methods
Animals and Management
Bos indicus steers (n = 32, 2 yr of age, 193 ± 21.47 kg mean BW) were halter-broken and taught to lead. The steers were ranked on BW, allocated to individual stalls at random, and fed a commercial forage cube (ME 8.5 MJ/kg DM, 12.5% CP, and 31.1% crude fiber [DM basis]; Cane Fiber Products, Brandon, Queensland, Australia) ad libitum for 14 d before the commencement of the experiment. All experimental procedures were reviewed and approved by the animal ethics committee at James Cook University (Approval No. A664-01).
Treatments
Animals were assigned randomly in a 2 x 2 factorial arrangement to one of four groups: 1) no water/no cortisol, n = 8; 2) water/no cortisol, n = 8; 3) no water/cortisol, n = 8; and 4) water/cortisol, n = 7). On d -1, all animals were catheterized with a polyvinyl chloride tube (o.d. 2.0 mm x i.d. 1.0 mm; Critchley Electrical Products Pty. Ltd., Silverwater, NSW, Australia) inserted into the jugular vein under local anesthetic. All animals allocated to the two cortisol groups were given 0.1 mg•kg BW-1•h-1 of hydrocortisone (Solucortef, Upjohn Pty. Ltd., Rydalmere, NSW, Australia) suspended in isotonic saline administered at a rate of 0.1 mL•kg BW-1•h-1, for the duration of the experiment. The noncortisol groups were given an equivalent placebo infusion of isotonic saline. Animals that were in water-deprived groups had their water withdrawn at the commencement of the experiment. One steer was removed early in the experiment due to injury. Sixteen steers were allocated randomly to be fitted with canvas urine collectors 21 d before initiation of experimentation to minimize stress during sample collection. Urine collectors were fitted to animals at the start of the study (no water/no cortisol, n = 3; water/no cortisol, n = 3; no water/cortisol, n = 4; water/cortisol, n = 6).
Sample Collection
On d 0, 20 mL of blood was collected from all treatment groups and decanted into 2 x 10 mL tubes containing lithium heparin (Disposable Products Pty. Ltd., Adelaide, SA, Australia). The catheters were then flushed with 10 mL of heparinized saline (15,000 IU heparin•L-1 0.9% [wt/vol] saline) to prevent clotting between sampling periods. The sampling regimen for cortisol concentration continued at 6-h intervals for 90 h. All other analytes were sampled at 24-h intervals until 90 h. Total urine excreted was collected and measured every 24 h. Blood samples were immediately placed into an ice water slurry and then centrifuged at 200 x g for 15 min, and plasma was poured off within 2 h and frozen (-20°C) for analysis.
Urea, Electrolyte, and Metabolite Measurement
Analysis of Na and K in steer plasma was conducted using ion selective electrodes (Lablyte System 830, Beckman Instruments Inc., Brea, CA). Plasma Ca, P, Cl, total protein, and albumin were analyzed spectrophotometrically using a Cobas-Mira Autoanalyzer (Roche Diagnostics, Brisbane, QLD, Australia) with standard enzymatic and spectrophotometric kits (Ca, Catalog No. TR29248; P, Catalog No. TR30025; Cl, Catalog No. TR38025; total protein, Catalog No. TR34025; albumin, Catalog No. TR36025; Trace Scientific Ltd., Noble Park, VIC, Australia). Plasma urea nitrogen was analyzed with a Technicon Autoanalyzer 2 (Bran + Leubbe Pty. Ltd., Homebush, NSW, Australia) according to the Technicon autoanalyzer method SE40001FD4 (Bran + Leubbe Pty. Ltd.). Hematocrit was measured using a microcentrifuge (Quantum Scientific, Milton, QLD, Australia). Plasma osmolality was measured using an automatic osmometer (Knauer Osmometer, Berlin, Germany).
Plasma cortisol concentration was measured using a RIA kit (Spectria Cortisol 125I-coated tube kit, Orion Corp., Espoo, Finland). Plasma AVP and angiotensin II (AII) concentrations were assayed using RIA by Austin Biomedical services (Prosearch International Australia Pty. Ltd., Melbourne, VIC, Australia). Intra- and interassay coefficients of variation were 8 and 12%, respectively, for both AVP and AII hormone assays. Urea space measurements were determined at 0, 24, 48, 72, and 90 h for each animal using the technique described by Preston and Kock (1973). Total body water was recorded as the pool available to the urea molecule.
Statistical Analysis
Data for a 2 x 2 factorial arrangement of treatments, with the main effects for water (water vs. no water) and cortisol (cortisol infusion vs. no cortisol) and the interaction effects between water and cortisol, and sampling time, were analyzed statistically with a repeated measures ANOVA using Version 10 of the Statistical Package for Social Sciences (SPSS Inc., Chicago, IL). Quantitative variables (plasma electrolytes, plasma cortisol, AVP, AII, total protein, glucose, total body water, hematocrit, water intake, and urine output) were independently sampled. Tests for sphericity and homogeneity were conducted to test assumptions for the repeated measures ANOVA and, in all cases, these assumptions were satisfied. Least squares means and standard errors were presented and multiple comparison tests within factors were not performed because there were fewer than three groups and therefore any difference would be clearly perceived. Differences were considered significant when P < 0.05. Due to the secretion pattern of the cortisol concentrations in the no-water/no-cortisol group (Figure 1), a one-way ANOVA was performed based on the areas under the time curve, integrated using the multiple-application trapezoidal rule for the 30- to 60-h and the 60- to 90-h periods.
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Plasma Cortisol Concentration
Plasma cortisol concentrations from Bos indicus genotypes exposed to transport stress of 24.2 km, have ranged from 25 to 35 ng/mL when taken 1 h after transport (Lay et al., 1996). Other authors have reported physiological cortisol concentrations in cattle to range from a baseline of 0.5 to 9.0 ng/mL (Grandin, 1997) to extreme stress of 120 ng/mL (Locatelli et al., 1989). The cortisol concentrations of the cortisol-infused groups in the present study could arguably reflect a pharmacological rather than a physiological dose rate with a range of 276 to 442 ng/mL of plasma in the cortisol-infused groups throughout the experimental period.
Finberg et al. (1978) and Parker et al. (2003) demonstrated that water deprivation alone was not a prototypical stressor that will activate the HPA axis and elevate plasma cortisol in the camel and sheep, respectively. However, the concentrations of cortisol in the no-water/no-cortisol group began to increase at 60 h and remained relatively high the rest of the experimental period (Figure 1
). The peak plasma cortisol concentrations for the no-water/no-cortisol and the water/no-cortisol groups (51.65 ± 17.88 ng/mL and 16.80 ± 4.42 ng/mL) were recorded at 60 h and 66 h respectively. The area under the cortisol concentration curve during the 60- to 90-h period was higher (P = 0.028) for the no-water/no-cortisol group than the water/cortisol group. There were no differences among groups for area under the cortisol curve during the 30- to 60-h period.
Matthews and Parrott (1991) suggested a physiological interaction between stress, dehydration, and HPA function, in that HPA axis activity becomes sensitized to stressors as dehydration ensues. Their claim is supported by others who have indicated that endogenous AVP is of physiological importance in amplifying the ACTH response to stress (Redekopp et al., 1985). This evidence has significant animal welfare implications, in that the dehydration associated with long-distance transportation becomes a circumstance of aggravation to transport and handling stressors, resulting in higher HPA axis responses than if the animals were well hydrated.
Although it is likely that the hypothesis of Matthews and Parrott (1991) may explain the increased cortisol concentrations from a novel stimuli, after 60 h in the present study, the observed changes in the no-water/no-cortisol group may not necessarily be indicative of a HPA axis response to a stressor per se but rather to the very high levels of AVP and AII expressed in these animals. Because AVP and AII are potent vasoconstrictors, it may be possible that endogenous cortisol levels increased in these animals to prevent excessive vasoconstrictive effects of these water-retentive hormones (Sapolsky et al., 2000).
Arginine Vasopressin
Plasma AVP concentrations increased with time (P < 0.006) for all animals deprived of water between 0 and 24 h, 24 and 48 h, and 48 and 72 h (Figure 2). A cortisol x water x time interaction (P = 0.027) occurred between 48 and 72 h, indicating that the no-water/no-cortisol group demonstrated a greater AVP concentration as compared with the no-water/cortisol group. Aubury et al. (1965) reported that cortisol increased the osmotic threshold for AVP release in humans. This was demonstrated in the present study at 72 h only. At all other times, there were no differences between AVP concentrations in the water-deprived groups.
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demonstrated in camels an increase within 24 h of 5.3 ± 2.2 pg/mL that did not change for the rest of their water-deprivation period of 14 d (5.7 ± 2.2 pg/mL).
Arginine vasopressin may stimulate ACTH secretion and potentiate the response to corticotropin-releasing factor (Redekopp et al., 1985; Redekopp et al., 1986; Rittmaster et al., 1987). This effect has caused some authors to label AVP as a stress hormone. However, AVP may not mediate ACTH responses to all stressors (Irvine et al., 1989), and, in some cases, stressors have reduced plasma AVP levels (Keil and Severs, 1977). Parrott et al. (1987) reported that short-term isolation stress in sheep resulted in a negative relationship between cortisol and AVP. Greater cortisol concentrations were associated with lesser AVP concentrations; however, this relationship was not significant. Similarly, El-Nouty et al. (1980) demonstrated an increase in AVP with heat stress in cows but did not detect changes in glucocorticoids. This differs from other authors’ results, which showed that increased plasma cortisol was associated with a decreased urine output with longer term environmental stressors, suggestive that cortisol increases AVP concentrations or alternatively that cortisol has a mineralocorticoid effect (Guerrini and Bertchinger, 1982). Exogenous cortisol had little effect on the concentration of AVP in the plasma of Bos indicus steers in the present study. Water deprivation, however, had a consistent effect in increasing AVP concentrations.
Angiotensin II
A cortisol x water x time interaction occurred between 0 and 24 h (P < 0.001) and 48 and 72 h (P = 0.083) of the experimental period, demonstrating an increase in AII concentrations for the no-water/no-cortisol group compared with the other groups. Water x time interactions between 0 and 24 h (P < 0.001), 24 and 48 h (P = 0.053), and 48 and 72 h (P = 0.053) demonstrated increases in AII concentrations compared with the groups offered water ad libitum. However, the no-water/no-cortisol group largely influenced this effect. Cortisol x time interactions between 6 and 24 h (P < 0.001) and 48 and 72 h (P = 0.036) demonstrated a decrease in AII concentrations with the infusion of exogenous cortisol. The no-water/cortisol group maintained the same AII concentrations as the water/no-cortisol group, and the water/cortisol group’s AII concentration was below that of the water/no-cortisol group at 24 h (Figure 3).
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). Although acute hypovolemic stress consistently activates the HPA and RAA axes along with AVP and catecholamine secretion, lesser degrees of fluid loss result in inconsistent hormonal secretory patterns (Espiner, 1987). Angiotensin II has a tropic action on the kidney to retain Na and water as well as stimulating the production of aldosterone from the adrenals. The repeated treatment with ACTH or glucocorticoids results in a diminished response of the adrenal glomerulosa and in the suppression of rennin (Coghlan et al., 1979). Changes in Na status appear to be the predominant factor in the suppression of AII associated with excess cortisol infusion in the present study and in that of Coghlan et al. (1979). The hypernatremia that accompanies dehydration has also been implicated for the disruption of the nexus between the renin-angiotensin system and aldosterone in the sheep and camel (Blair-West et al., 1972; Ben Goumi et al., 1993). In the presence of a concurrent water deprivation, the complexity of endocrine interactions associated with water balance results in a homeostasis that occurs regardless of a deficit in one of the physiological systems employed. Cortisol has a suppressive effect on the RAA axis; however, our results are consistent with previous reports that, in the presence of water deprivation, it serves to protect and maintain water balance in times of stress (Parrott et al., 1987; Parker et al., 2003).
Urine Output
There was a cortisol x water x time (P = 0.057) interaction, between 48 and 72 h of the treatment period, demonstrating that the water/cortisol group maintained urine output for 48 h and then decreased their urine output at 72 h of the treatment period (Figure 4). Glucocorticoids have been shown to antagonize the effects of AVP by increasing the glomerular filtration rate (De Matteo and May, 1999) and the secretion of atrial natriuretic peptide. Baas et al. (1984) indicated that the mechanism in which pharmacological doses of cortisol induced a polyuria in the dog was due to an inhibition of the action of AVP, causing decreased water and urea reabsorption by the kidney. Their findings were associated with polydipsia in well-hydrated animals. Similarly, a diuresis was also found in well-hydrated sheep offered ad libitum water, and given stress-like infusions of cortisol. However, when sheep were water deprived and infused with cortisol, the diuretic effect ceased (Parker et al., 2003). Concentrations of AVP and AII were not elevated in the water/cortisol group, which would allow a diuresis to occur via an increase in the glomerular filtration rate. After 48 h of the treatment period, the decrease seen in the urine production of this group may have been associated with the mineralocorticoid effect of cortisol on the steers causing Na and water retention.
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). The decrease in osmolality at 72 h for all groups may have been due to fluctuations in water compartments within the animal.
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Although hematocrit data remained within normal physiological limits for all groups, there was a water x cortisol x time interaction at 90 h (P = 0.028) of the treatment period, demonstrating that the water/cortisol group had lesser hematocrit as compared with the water-deprived groups at 90 h (Figure 6). Hematocrit data did not indicate dehydration in any group.
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concluded that urea space was proportional to empty body water (total body water less the water in the gastrointestinal tract). We previously reported that the replacement of water from the gastrointestinal tract may have been responsible for maintenance of body water in Merino sheep in the presence of a cortisol-induced diuresis (Parker et al., 2003). Data supporting the body water assay appear to be ambiguous. The results for AVP and AII in the present study indicate a loss of water from the vascular space in the water-deprived groups, especially the no-water/no-cortisol group. This is supported by a time x water effect on plasma osmolality in the water-deprived groups. In contrast to this, the hematocrit, total protein, and albumin data indicated no difference among groups in the present study. The water pools in the ruminant body are dynamic, moving freely from the lumen of the gastrointestinal tract to the extracellular fluid. This flux has resulted in considerable variation in the determination of body water loss from stressors (Cole, 1995). Other procedural considerations in undertaking the urea space assay have been implicated by Bartle et al. (1988) as significant sources of error. However, we are confident that sampling and analytical errors were minimized in the present study. It would appear that during 90 h of water deprivation, Bos indicus steers were able to utilize sufficient water from the gastrointestinal tract to prevent a decrease in empty body water content.
Plasma Electrolytes
Plasma Na concentrations had water x time interactions between 0 and 24 h (P = 0.014), 48 and 72 h (P = 0.022), and 72 and 90 h (P = 0.076) of the treatment period (Figure 7), indicating that water-deprived animals had greater plasma Na concentrations as compared with animals that had access to water. The no-water/cortisol group had the greatest plasma sodium concentrations of all the groups from 24 h of the treatment period until the completion of the experiment. Despite the pharmacological dose rate given to the cortisol-infused animals in the present study, water deprivation alone had a greater effect on plasma Na concentration.
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). The difference between the cortisol and no-cortisol groups was maintained until 90 h of the treatment period when the no water/no-cortisol group had decreased its plasma K to the same extent as the cortisol groups. The pre- and post-ANOVA performed on data collected at 60 h of the treatment period for cortisol concentration in the no-water/no-cortisol group demonstrated an increase in the concentration of endogenous cortisol after 60 h (Figure 1). This increase may have been sufficient to induce the decrease in plasma K. Alternatively, Bianca et al. (1965) reported a similar effect and proposed the reduced feed intake to have decreased plasma K concentrations.
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). The decreased feed intake caused by water deprivation and the subsequent effects on gastrointestinal motility and absorption in the water-deprived groups did not have a significant effect on plasma concentrations of Ca until 90 h. The plasma concentrations of Ca in the no-water/no-cortisol group were 1.75 mmol/L ± 0.12 mmol/L at 90 h of the experimental period, which falls below the range for Ca in cattle of 2.00 to 2.62 mmol/L (Blood and Radostits, 1989), although all other groups were within the normal range.
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). Plasma concentrations and interactions of main effects with time on Cl concentrations followed Na concentrations in plasma. All groups were within normal ranges for plasma Cl in cattle (95 to 110 mmol/L) (Blood and Radostits, 1989).
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). The plasma P concentration of the cortisol groups remained within normal limits for cattle of 1.30 to 2.25 mmol/L (Blood and Radostits, 1989).
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). However, the watered groups did not alter their feed intake throughout the study. High-cortisol concentrations in sheep may reduce water intake or cause complete abstinence from drinking (Guerrini and Bertchinger, 1982; Parrott et al., 1987). The water/cortisol group failed to repeat the behaviors reported by Guerrini and Bertchinger (1982) and Parrott et al. (1987). The isolation and/or restraint stress in previous experiments may have activated the SAM and HPA axes, resulting in a number of neuroendocrine products that collectively may have altered drinking behavior. This suggests that excess cortisol alone is not responsible for the fluctuations in water intake in the present study. Data for feed intake indicated a time x water interaction between 0 and 24 h (P = 0.005), 24 and 48 h (P = 0.032), and 72 and 90 h (P = 0.013) of the treatment period, demonstrating a decreased feed intake from the water-deprived groups as compared with the groups offered water ad libitum.
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In the presence of water deprivation, the complexity of endocrine interactions associated with water balance results in homeostasis regardless of a deficit in one of the physiological systems employed. Excess cortisol has a suppressive effect on the renin-angiotensin-aldosterone axis; however, it does not affect the circulating concentrations of arginine vasopressin. Plasma electrolytes, in the present study, demonstrated small but significant changes over time; however, electrolytes and metabolite concentrations remained within physiologically normal range limits. In the presence of water deprivation, cortisol may serve to protect and maintain water balance in times of stress.
Footnotes
1 This project was jointly funded by James Cook University, the Australian Live Export Corporation, and Meat and Livestock Australia. 
2 Correspondence—e-mail: lee.fitzpatrick{at}jcu.edu.au.
Received for publication June 7, 2003. Accepted for publication November 18, 2003.
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) steer groups. The no-water/no-cortisol group demonstrated a group x time interaction (P = 0.028) toward increasing the area under the plasma cortisol concentration curve from 60 to 90 h compared with the water/no-cortisol group.
