Effects of cortisol secreted via a 12-h infusion of adrenocorticotropic hormone on mineral homeostasis and bone metabolism in ovariectomized cows

To evaluate the effects of endogenously secreted cortisol on mineral homeostasis and bone metabolism in cows, 4 ovariectomized Holstein cows were infused for 12 h with either an adrenocorticotropic hormone (ACTH) solution (0.5 mg/2 L isotonic NaCl solution per cow) or isotonic NaCl solution in a 2 × 2 crossover design. ACTH infusion stimulated cortisol secretion and increased plasma cortisol concentrations for 18 h (P < 0.001), leading to an elevated plasma glucose concentration until 36 h (P < 0.001). Plasma calcium and magnesium concentrations in ACTH-infused cows fluctuated within normal ranges, whereas hypophosphatemia was observed unequivocally. The biochemical bone resorption markers tartrate-resistant acid phosphatase 5b and hydroxyproline decreased following ACTH infusion (P < 0.001 and P = 0.003, respectively). Similarly, the bone formation marker, bone-specific alkaline phosphatase, decreased continuously until 72 h after the ACTH infusion (P < 0.001). These results demonstrate that increased secretion of cortisol via a 12-h ACTH infusion disrupted homeostasis of inorganic phosphate and suppressed bone metabolism in ovariectomized cows without involving gonadal steroid hormones.     

Circulating β-endorphin,adrenocorticotrophic hormone and cortisol levels of stallions before and after short road transport: stress effect of different distances

Background

Since transport evokes physiological adjustments that include endocrine responses, the objective of this study was to examine the responses of circulating β-endorphin, adrenocorticotrophic hormone (ACTH) and cortisol levels to transport stress in stallions.

Methods

Forty-two healthy Thoroughbred and crossbred stallions were studied before and after road transport over distances of 100, 200 and 300 km. Blood samples were collected from the jugular vein: first in a single box immediately before loading (pre-samples), then immediately after transport and unloading on arrival at the breeding stations (post-samples).

Results

An increase in circulating β-endorphin levels after transport of 100 km (P < 0.01), compared to basal values was observed. Circulating ACTH levels showed significant increases after transport of 100 km (P < 0.001) and 200 km (P < 0.001). Circulating cortisol levels showed significant increases after road transport over distances of 100, 200 and 300 km (P < 0.001). An effect of transport on β-endorphin, ACTH and cortisol variations was therefore evident for the different distances studied. No significant differences (P > 0.05) between horses of different ages and different breeds were observed for β-endorphin, ACTH and cortisol levels.

Conclusion

The results obtained for short term transportation of stallions showed a very strong reaction of the adrenocortical system. The lack of response of β-endorphin after transport of 200–300 km and of ACTH after transport of 300 km seems to suggest a soothing effect of negative feedback of ACTH and cortisol levels.     

Endocrine responses of healthy parrots to ACTH and thyroid stimulating hormone

Effects of exogenous ACTH on plasma corticosterone and cortisol concentrations and the effects of thyroid stimulating hormone (TSH) on plasma triiodothyronine (T3) and thyroxine (T4) were determined in the following 3 species of parrots: red-lored Amazon (group 1), blue-fronted Amazon (group 2), and African gray (group 3). Each bird was given ACTH (0.125 mg/bird) IM, except for 3 to 4 birds in each group, which were given saline solution (controls). Blood samples were collected before and 90 minutes after ACTH stimulation. In group 1 (n = 12), mean plasma corticosterone concentrations increased significantly (P less than 0.001) from 1.06 microgram/dl (before ACTH) to 4.89 micrograms/dl (after ACTH); mean corticosterone concentrations increased in the control birds from 1.06 microgram/dl to 1.84 microgram/dl; and mean cortisol concentrations increased only slightly from 0.228 microgram/dl to 0.266 microgram/dl. In group 2 (n = 12), mean corticosterone concentrations increased significantly (P less than 0.001) from 2.09 micrograms/dl to 10.58 micrograms/dl; control mean corticosterone concentrations decreased slightly from 2.09 micrograms/dl to 1.77 microgram/dl; and mean cortisol concentrations increased from less than or equal to 0.16 microgram/dl to 0.266 microgram/dl. In group 3 (n = 12), mean plasma corticosterone concentrations increased significantly (P less than or equal to 0.001) from 2.33 micrograms/dl to 4.67 micrograms/dl; mean control plasma corticosterone concentrations decreased from 2.33 micrograms/dl to 1.68 microgram/dl; and plasma corticol concentrations were not detectable. Each bird was given TSH, IM (1 U/bird). Blood samples were collected before and 6 hours after TSH administration. Saline solution was not administered as controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adrenocortical Response in Cows after Intramuscular Injection of Long‐Acting Adrenocorticotropic Hormone (Tetracosactide Acetate Zinc Suspension)

The objectives of this study were first to show adrenocortical response to a long‐acting adrenocorticotropic hormone preparation (tetracosactide acetate zinc suspension) (ACTH‐Z) and its effect on adrenocortical function in beef cows ( Experiment 1 ) and second to apply the ACTH‐Z challenge in dairy cows based on cortisol concentrations in milk collected at routine milking ( Experiment 2 ). In Experiment 1 , four beef cows in luteal phase were challenged with ACTH‐Z, and plasma cortisol concentrations were determined for 48 h after the injection at 30‐min to 2‐h intervals. A rapid ACTH test was conducted 3 days before and 2 h after the completion of ACTH‐Z injection for 48 h to investigate the effect on adrenocortical function. Plasma cortisol concentrations increased significantly 30 min after ACTH‐Z injection (p < 0.001), and the high cortisol levels were maintained for approximately 10 h after the injection. In Experiment 2 , eight dairy cows were subjected to ACTH‐Z challenge 1–2 weeks and 4–5 weeks post‐partum. Blood and milk samples were taken at morning and afternoon milking. All the cows showed a significant increase in cortisol concentrations in plasma as well as in skim milk 8 h after ACTH‐Z injection 1–2 weeks and 4–5 weeks post‐partum (p < 0.001). There was a significant correlation between plasma and skim milk cortisol concentrations 8 h after ACTH‐Z challenge (r = 0.74, p < 0.001). The results obtained in this study suggest that elevated levels of plasma cortisol are maintained for approximately 10 h after ACTH‐Z treatment without adverse effect on adrenocortical function and a long‐acting ACTH‐Z challenge based on cortisol concentrations in milk, which were collected at the morning and the afternoon milking, can be a useful tool to monitor adrenocortical function in cows.     

ACTH stimulation test in the captive cheetah (Acinonyx jubatus)

Serum cortisol response was assessed in 8 captive cheetahs, of varying ages, after the intravenous administration of 500 microg of tetracosactide (Synacthen Depot, Novartis, Kempton Park) while maintained under general anaesthesia. In addition, 8 cheetahs were anaesthetised and given an equal volume of saline in order to establish baseline cortisol concentrations at similar stages of anaesthesia. A significant difference in the median cortisol concentration measured over time was found following ACTH administration in the ACTH group (P < 0.001). There was no difference between the median cortisol concentrations in the ACTH group at time-points 120, 150 and 180 min after ACTH stimulation (P = 0.867). Thus it appears appropriate to collect serum 120 to 180 min after tetracosactide administration to assess maximal stimulation of the adrenal in the cheetah. No statistically significant rise was seen in the anaesthetised control group following the injection of saline (P = 0.238).     

Cortisol secretion after adrenocorticotrophin (ACTH) and Dexamethasone tests in healthy female and male dogs

Background

For the conclusive diagnosis of Cushing''s Syndrome, a stimulating ACTH test or a low suppressive Dexamethasone test is used. Reports in other species than the dog indicate that plasma cortisol concentration after ACTH administration is affected by gender. We investigated the effect of gender on the cortisol response to ACTH and Dexamethasone tests in dogs.

Methods

Seven healthy adult Cocker Spaniels (4 females and 3 males) were assigned to a two by two factorial design: 4 dogs (2 females and 2 males) received IV Dexamethasone 0.01 mg/kg, while the other 3 dogs received an IV saline solution (control group). Two weeks later the treatments were reversed. After one month, ACTH was given IV (250 μg/animal) to 4 dogs (2 female and 2 males) while the rest was treated with saline solution (control group). Cortisol concentrations were determined by a direct solid-phase radioimmunoassay and cholesterol and triglycerides by commercial kits.

Results and Discussion

No effect of treatment was observed in metabolite concentrations, but females presented higher cholesterol concentrations. ACTH-treated dogs showed an increase in cortisol levels in the first hour after sampling until 3 hours post injection. Cortisol concentrations in Dexamethasone-treated dogs decreased one hour post injection and remained low for 3 hours, thereafter cortisol concentrations increased. The increase in cortisol levels from one to two hours post ACTH injection was significantly higher in females than males. In Dexamethasone-treated males cortisol levels decreased one hour post injection up to 3 hours; in females the decrease was more pronounced and prolonged, up to 5 hours post injection.

Conclusion

We have demonstrated that cortisol response to ACTH and Dexamethasone treatment in dogs differs according to sex.     

Adrenocortical response to ACTH in Angora and Spanish goat wethers.

Angora goats do not cope well with stress compared with goats of other breeds. Our hypothesis that this involves subclinical primary hypoadrenocorticism associated with low cortisol release in response to ACTH stimulation was tested by measuring adrenocortical response (plasma cortisol) in six Spanish (37 +/- 2 kg BW) and six Angora wethers (39 +/- 3 kg BW) under simulated acute and chronic ACTH challenges. In Exp. 1 (acute ACTH challenge), wethers were dosed i.v. with high (2.5 IU/kg BW) or low (.4 IU/kg BW) quantities of ACTH. In Exp. 2 (chronic ACTH challenge), ACTH at the rate of .015 IU/(kg BW x min) or saline (.15 M NaCl) was infused i.v. at 15 mL/h for 6 h. The mean baseline plasma cortisol concentration before ACTH stimulation was similar (P > .05) between Angora and Spanish goats in Exp. 1 (averaged over days) and in Exp. 2. The cortisol concentration response area (ng/ (mL x min) x 10(-3)) above the baseline was similar (P > .05) between Angora and Spanish goats during low (7.6 +/- .5 and 9.0 +/- 1.7, respectively) and high (12.8 +/- 1.0 and 16.0 +/- 1.8, respectively) levels of acute ACTH challenge (Exp. 1) and during chronic ACTH challenge (45.1 +/- 5.9 and 41.8 +/- 7.3, respectively; Exp. 2). In conclusion, these data indicate that, under the conditions of this study, adrenocortical responsiveness to ACTH stimulation is not different between Angora and Spanish goat wethers and, thus, may not contribute to stress susceptibility in Angora goats.     

Assessment of adrenal function in cats: Response to intravenous synthetic ACTH

The serum cortisol response to intravenous synthetic ACTH (tetracosactrin) was assessed in 15 healthy adult cats. Mean cortisol levels showed a significant (P<0.001) rise at 60 minutes and peaked at 180 minutes. At 120 and 180 min- utes mean cortisol levels were significantly (P<0.001) higher than at 60 minutes. The time of peak cortisol response in individual cats varied between 120 and 240 minutes, but nine (60 per cent) peaked at 180 minutes. In response to the ACTH the cats showed a rise in cortisol levels of between 160 and 1360 per cent. No significant rise in cortisol levels was seen in five cats following administration of sterile saline.     

Adrenal function in the cat: comparison of the effects of cosyntropin (synthetic ACTH) and corticotropin gel stimulation

The serum cortisol responses of 10 normal cats to natural adrenocorticotrophic hormone (ACTH) gel and synthetic ACTH (cosyntropin) were evaluated and compared. Following administration of either ACTH gel or cosyntropin, mean serum cortisol concentrations increased significantly (P less than 0.05) within 30 minutes and reached a maximal response (2.5 to 10 times basal values) at 90 minutes. The time to reach peak serum cortisol concentrations was variable, however, and occurred sooner after cosyntropin (30 to 60 minutes) than after ACTH gel administration (90 to 180 minutes). While ACTH gel tended to produce a prolonged cortisol response, the effects of cosyntropin were more transient, with serum cortisol concentrations returning to normal range within three hours after injection. Results of this study indicate that the administration of either ACTH gel or cosyntropin consistently produces an adequate adrenocortical response in the cat. Based on the time response studies, post ACTH cortisol samples should be collected 60 to 90 minutes after cosyntropin or 90 to 120 minutes after ACTH gel injection to ensure detection of peak adrenocortical response with either ACTH preparation.     

Ovarian localization of 11β-hydroxysteroid dehydrogenase (11βHSD): effects of ACTH stimulation and its relationship with bovine cystic ovarian disease

Cystic ovarian disease (COD) is an important cause of infertility in cattle, and ACTH has been involved in regulatory mechanisms related to ovarian function associated with ovulation, steroidogenesis, and luteal function. Here, we examined the localization of 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) and 11βHSD2 proteins in the ovary of healthy cows and animals with spontaneous and ACTH-induced COD and the in vitro response of the follicular wall exposed to ACTH. After stimulation by ACTH, we documented changes in 11βHSD expression and cortisol secretion by the follicular wall of large antral and follicular cysts. Follicular cysts showed a higher constitutive expression of both enzymes, whereas ACTH induced an increase in 11βHSD1 in tertiary follicles and follicular cysts and a decrease in 11βHSD2 in follicular cysts. Moderate expression of 11βHSD1 was observed by immunohistochemistry in granulosa of control animals, with an increase (P < 0.05) from primary to secondary, tertiary, and atretic follicles. The level of immunostaining in theca interna was lower than that in granulosa. The expression of 11βHSD2 was lower in the granulosa of primary follicles than in that of secondary, tertiary, and atretic follicles and was lower in the theca interna than in the granulosa. In ACTH-induced and spontaneously occurring follicular cysts, differences from controls were observed only in the expression of 11βHSD1 in the granulosa, being higher (P < 0.05) than in tertiary follicles. These findings indicate that follicular cysts may be exposed to high local concentrations of active glucocorticoids and indicate a local role for cortisol in COD pathogenesis and in regulatory mechanisms of ovarian function.     

Effect of ACTH on plasma corticosterone and cortisol in eagles and condors

The effect of ACTH on plasma corticosterone and cortisol was determined in 12 eagles (Haliaeetus leucocephalus) and in 6 Andean condors (Vultur gryphus). In all raptors, the concentration of plasma corticosterone was substantially greater than that of cortisol. After ACTH administration, the eagles had a marked increase (P less than 0.001) in plasma corticosterone concentrations, but not in plasma cortisol. Administration of saline solution did not induce increased plasma corticosterone concentrations in the eagles. The condors had a smaller increase (P less than 0.002) in plasma corticosterone concentrations after ACTH administration, as compared with that of the eagles. However, administration of saline solution in 2 condors resulted in an increase in corticosterone similar to the increase after ACTH administration. In the condor, a stress-related release of endogenous ACTH may have an effect similar to that induced by exogenously administered ACTH. Plasma cortisol concentrations did not increase significantly after administration of ACTH or saline solution in either raptor species.     

Induced gonadotropin release in adrenocorticotropin-treated bulls and steers

The effect of adrenocorticotropin hormone (ACTH) on plasma cortisol and on gonadotropin releasing hormone (GnRH)-induced release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone was determined in nine Holstein bulls and 12 Holstein steers. Treatments consisted of animals receiving either GnRH (200 micrograms, Group G), ACTH (.45 IU/kg BW, Group A) or a combination of ACTH followed 2 h later by GnRH (Group AG). Group G steers and bulls had elevated plasma LH and FSH within .5 h after GnRH injection and plasma testosterone was increased by 1 h after GnRH injection in bulls. In Group A, plasma cortisol was elevated by .5 h after ACTH injection in both steers and bulls, but plasma LH and FSH were unaffected. In Group A bulls, testosterone was reduced after ACTH injection. In Group AG, ACTH caused an immediate increase in plasma cortisol in both steers and bulls, but did not affect the increase in either plasma LH or FSH in response to GnRH in steers. In Group AG bulls, ACTH did not prevent an increase in either plasma LH, FSH or testosterone in response to GnRH compared with basal concentrations. However, magnitude of systemic FSH response was reduced compared with response in Group G bulls, but plasma LH and testosterone were not reduced. The results indicate that ACTH caused an increase in plasma cortisol, but did not adversely affect LH or FSH response to GnRH in steers and bulls. Further, while testosterone was decreased after ACTH alone, neither ACTH nor resulting increased plasma cortisol resulted in decreased testosterone production in the bull after GnRH stimulation.     

Effects of adrenocorticotropic hormone and flunixin meglumine on pregnancy retention in beef cows

Pregnancy loss in beef cattle after d 28 of gestation is variable, but it has been reported to be as great as 14% and has been related to transportation or handling stress. The primary objective of this study was to determine whether activation of the hypophyseal-adrenal axis with ACTH would mimic a stressful response and cause pregnancy loss in beef cattle. A secondary objective was to determine if a single injection of the PG synthesis inhibitor flunixin meglumine would attenuate the stress response and suppress serum PGF(2α) concentrations to prevent pregnancy loss. Forty nonlactating beef cows that were 34 ± 0.33 d pregnant were used for this study. In a 2 × 3 factorial arrangement, cows were randomly assigned to receive ACTH [0 or 0.5 IU/kg of BW, intramuscularly (i.m.)] at 0 and 2 h of the study and flunixin meglumine (0, 1.1, or 2.2 mg/kg of BW, i.m.) at 0 h. Blood samples were collected from all cows at 0 h and every 30 min for 4 h to measure serum cortisol and PGF(2α) metabolite (PGFM) concentrations. Rectal temperature was collected for each cow at 0, 120, and 240 min. Pregnancy exams were conducted 31 and 58 d after treatment by transrectal ultrasonography, and the presence of a fetal heartbeat was used as an indicator of fetal viability. Serum cortisol concentration was affected (P < 0.01) by ACTH, time, and the interaction of ACTH × time, but not by flunixin meglumine (P ≥ 0.14) or any other interactions. Cortisol concentrations increased (P < 0.01) in the serum of ACTH-treated cows immediately after ACTH treatment and remained increased (P < 0.01) throughout the 4-h sampling period. Serum PGFM concentration was not affected by ACTH (P = 0.97) or by any interactions (P > 0.35) with ACTH, but was affected (P < 0.01) by flunixin meglumine, time, and the interaction of flunixin meglumine × time. Regardless of dosage (1.1 or 2.2 mg/kg of BW), flunixin meglumine decreased (P < 0.01) serum PGFM concentrations in both ACTH-treated and control cows for the duration of the study. Although ACTH treatment induced a prolonged increase in serum cortisol concentration, none of the cows used in this study lost a pregnancy. In conclusion, the activation of the hypophyseal-adrenal axis with ACTH increased serum cortisol concentrations but did not increase serum concentrations of PGFM or cause pregnancy loss during early gestation in cows. Flunixin meglumine treatment suppressed serum PGFM concentrations in control and ACTH-treated cows.     

Blood arginine vasopressin, adrenocorticotropin hormone, and cortisol concentrations at admission in septic and critically ill foals and their association with survival

BACKGROUND: Sepsis is an important cause for neonatal foal mortality. The hypothalamic-pituitary-adrenal axis (HPAA) responses to sepsis are well documented in critically ill humans, but limited data exist in foals. The purpose of this study was to evaluate the HPAA response to sepsis in foals, and to associate these endocrine changes with survival. HYPOTHESIS: Blood concentrations of arginine vasopressin (AVP), adrenocorticotropin hormone (ACTH), and cortisol will be higher in septic foals as compared with sick nonseptic and healthy foals. The magnitude of increase in hormone concentration will be negatively associated with survival. ANIMALS: Fifty-one septic, 29 sick nonseptic, and 31 healthy foals of < or =7 days of age were included. METHODS: Blood was collected at admission for analysis. Foals with positive blood culture or sepsis score > or =14 were considered septic. Foals admitted with disease other than sepsis and healthy foals were used as controls. AVP, ACTH, and cortisol concentrations were measured using validated immunoassays. RESULTS: AVP, ACTH, and cortisol concentrations were increased in septic foals. Septic nonsurvivor foals (n = 26/51) had higher plasma ACTH and AVP concentrations than did survivors (n = 25/51). Some septic foals had normal or low cortisol concentrations despite increased ACTH, suggesting relative adrenal insufficiency. AVP, ACTH, and cortisol concentrations were higher in sick nonseptic foals compared with healthy foals. CONCLUSIONS AND CLINICAL IMPORTANCE: Increased plasma AVP and ACTH concentrations in septic foals were associated with mortality. Several septic foals had increased AVP : ACTH and ACTH : cortisol ratios, which indicates relative adenohypophyseal and adrenal insufficiency.     

Cortisol responses to dehorning of calves given a 5-h local anaesthetic regimen plus phenylbutazone,ketoprofen, or adrenocorticotropic hormone prior to dehorning

The purpose of this work was to assess whether the non-steroidal anti-inflammatory drugs (NSAIDs) phenylbutazone and ketoprofen, and an adrenocorticotropic hormone (ACTH) induced cortisol surge, reduce the cortisol response which occurs when the local anaesthetic wears off in calves following dehorning. There were four control groups and one dehorned group; also four groups were given local anaesthetic lasting 5h and were dehorned without or with phenylbutazone, ketoprofen or an ACTH injection, one group was injected with ACTH twice (at 0 and 6h) and another received ACTH and 6h later was dehorned. Blood samples were taken before and after dehorning and plasma cortisol concentrations were determined by radio-immunoassay. Dehorning increased the mean plasma cortisol concentrations [max 137 (11)nmoll(-1)] above control values [38 (5)nmoll(-1)] for about 7h, whereas local anaesthesia maintained concentrations at control values until about 5h after dehorning, and then they became elevated until about 10h. The maximum rise in mean concentration which occurred when the local anaesthetic wore off [128 (32)nmoll(-1)] was not affected when phenylbutazone was given before dehorning [141 (28)nmoll(-1)], but was reduced significantly when ketoprofen [65 (17)nmoll(-1)] or ACTH [61 (19)nmoll(-1)] were injected before or at the time of dehorning, respectively. Marked cortisol responses to ACTH injected at 0 and 6h were similar, but the early part of the cortisol response to dehorning 6h after an ACTH injection was reduced. It is suggested that the delayed cortisol response, which began 5h after dehorning, arose both from ketoprofen-sensitive and cortisol-sensitive sensory input as well as from other factors. Phenylbutazone did not affect the sensory input from the amputation wounds in the present calves.     

Duration of pituitary and adrenocortical suppression after long-term administration of anti-inflammatory doses of prednisone in dogs.

Duration and magnitude of hypothalamic-pituitary-adrenal axis suppression caused by daily oral administration of a glucocorticoid was investigated, using an anti-inflammatory dose of prednisone. Twelve healthy adult male dogs were given prednisone orally for 35 days (0.55 mg/kg of body weight, q 12 h), and a control group of 6 dogs was given gelatin capsule vehicle. Plasma cortisol (baseline and 2-hour post-ACTH administration) and plasma ACTH and cortisol (baseline and 30-minutes post corticotropin-releasing hormone [CRH] administration) concentrations were monitored biweekly during and after the 35-day treatment period. Baseline plasma ACTH and cortisol and post-ACTH plasma cortisol concentrations were significantly (P less than 0.05) reduced in treated vs control dogs after 14 days of oral prednisone administration. By day 28, baseline ACTH and cortisol concentrations remained significantly (P less than 0.05) reduced and reserve function was markedly (P less than 0.0001) reduced as evidenced by mean post-CRH ACTH, post-CRH cortisol, and post-ACTH cortisol concentrations in treated vs control dogs. Two weeks after termination of daily prednisone administration, significant difference between group means was not evident in baseline ACTH or cortisol values, post-CRH ACTH or cortisol values, or post-ACTH cortisol values, compared with values in controls. Results indicate complete hypothalamic-pituitary-adrenal axis recovery 2 weeks after oral administration of an anti-inflammatory regimen of prednisone given daily for 5 weeks.     

Genetic linkage mapping of quantitative trait loci for behavioral and neuroendocrine stress response traits in pigs

A QTL analysis of behavioral and neuroendocrine responses to a "novel environment" stress was conducted in a three-generation experimental cross between Meishan and Large White pig breeds. A total of 186 F2 males and 182 F2 females were studied for their behavioral and neuroendocrine reactivity to a novel environment test at 6 wk of age. Locomotion, vocalization, and defecation rate, as well as exploration time, were measured for 10 min. Blood samples were taken immediately before and after the test to measure plasma levels of ACTH, cortisol, and glucose. Animals were typed for a total of 137 markers covering the entire porcine genome. Analyses were performed using two interval mapping methods: a line-cross regression method, where founder lines were assumed to be fixed for different QTL alleles, and a half-/full-sib maximum likelihood method where allele substitution effects were estimated within each half-/full-sib family. Both methods revealed a highly significant gene effect for poststress cortisol level (P < 0.001) and a significant effect for basal cortisol level (P < 0.05) at the end of the q arm of chromosome 7, explaining, respectively, 20% and 7% of the phenotypic variance. Meishan alleles are associated with higher cortisol levels and are partially dominant (for poststress levels) over Large White alleles. Other significant gene effects on biological measures were detected on chromosomes 1 and 17 (ACTH response to stress), 3, 5, and 8 (glucose levels). The SSC 17 QTL explains 12% of the phenotypic variance of poststress ACTH levels, with a suggestive evidence of imprinting effects. Meishan alleles are associated with lower poststress ACTH levels. Gene effects of low amplitude only were found for behavioral reactivity traits. Considering the effects of stress neuroendocrine systems on energy fluxes and protein deposition, and the importance of stress reactivity for meat quality and animal welfare, these results open new perspectives for pig selection.     

The effect of active immunization against adrenocorticotropic hormone on cortisol, beta-endorphin, vocalization, and growth in pigs

Because the poor growth performance of intensively housed pigs is associated with increased circulating glucocorticoid concentrations, we investigated the effects of glucocorticoid suppression by inducing a humoral immune response to ACTH on physiological and production variables in growing pigs. Grower pigs (28.6 +/- 0.9 kg) were immunized with amino acids 1 through 24 of ACTH conjugated to ovalbumin and suspended in diethylaminoethyl (DEAE) dextran-adjuvant or adjuvant alone (control) on d 1, 28, and 56. The ACTH-specific antibody titers generated suppressed increases in cortisol concentrations on d 63 in response to an acute stressor (P = 0.002; control = 71 +/- 8.2 ng/mL; ACTH-immune = 43 +/- 4.9 ng/mL) without altering basal concentrations. Plasma beta-endorphin concentrations were also increased (P < 0.001) on d 63 (control = 18 +/- 2.1 ng/mL; ACTH-immune = 63 +/- 7.3 ng/mL), presumably because of a release from negative feedback on the expression of proopiomelanocortin in pituitary corticotropes. Immunization against ACTH did not alter ADG (P = 0.120; control = 1,077 +/- 25; ACTH-immune = 1,143 +/- 25 g) or ADFI (P = 0.64; control = 2,719 +/- 42; ACTH-immune = 2,749 +/- 42 g) and did not modify behavior (P = 0.681) assessed by measuring vocalization in response to acute restraint. In summary, suppression of stress-induced cortisol responses through ACTH immunization increased beta-endorphin concentrations, but it did not modify ADG, ADFI, or restraint vocalization score in growing pigs.     

Evaluation of plasma aldosterone concentrations before and after ACTH administration in clinically normal dogs and in dogs with various diseases

Plasma aldosterone concentrations were measured in response to adrenocorticotropic hormone (ACTH) gel administration in clinically normal dogs, in dogs with hypoadrenocorticism, and in dogs (with electrolyte abnormalities) that did not have hypoadrenocorticism. Baseline plasma aldosterone concentrations were determined from specimens obtained every 10 minutes for 3 hours from 2 dogs and every 30 minutes for 7.5 hours from 2 other dogs. During the evaluation period, plasma aldosterone concentrations varied by at least 50% in each dog. A randomized crossover design was used to compare changes in plasma aldosterone concentrations after administration of ACTH gel and physiologic NaCl solution. Dogs had significantly (P = 0.002) higher plasma aldosterone concentrations after administration of ACTH gel than after administration of NaCl solution. Plasma cortisol concentrations increased as expected after ACTH gel administration. Analysis of cortisol and aldosterone concentrations in the same specimens obtained at 7 sample collection times did not reveal significant linear correlation, and scatterplots did not indicate a nonlinear association. In addition, plasma aldosterone concentrations were determined in response to ACTH administration alone and to ACTH combined with a high dose of dexamethasone (0.1 mg/kg, IV). The plasma aldosterone response to ACTH alone was not significantly different from the response to ACTH combined with dexamethasone. For both tests, plasma aldosterone concentrations at 60 and 120 minutes after ACTH administration were significantly (P less than 0.0005 and P = 0.0001, respectively, increased, compared with base-line values. Six dogs with adrenocortical hypofunction, as determined by plasma cortisol concentrations before and after ACTH administration, had plasma aldosterone concentrations that were diminished or did not increase after ACTH administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Technical note: effect of corticotropin-releasing hormone on adrenocorticotropic hormone and cortisol in steers

The objective of this study was to determine an appropriate exogenous dose of bovine corticotropin-releasing hormone (bCRH) to stimulate the physiological effects of the hypothalamic-pituitary-adrenal axis in steers as a method to test the sensitivity of the pituitary and adrenal gland. Twenty 14-mo-old Holstein-Friesian steers were blocked by weight (443.7+/-2.5 kg) and randomly allotted to receive either saline (control) or bCRH (0.1, 0.3, 1.0, or 1.5 microg/kg BW). Animals were housed in a slatted-floor facility (n = 5 per pen). Indwelling jugular catheters, for both the administration of bCRH and blood collection, were fitted on d -1 of the experiment. Saline and bCRH were administered i.v. at time 0. Serial blood samples were collected at -15, 0, 15, 30, 45, 60, 75, 90, 105, 120, 135, 150, 165, and 180 min relative to time 0. Following administration of 0.1 microg of bCRH/kg BW, the peak ACTH response was not significantly different from pretreatment baseline concentrations (mean concentrations as measured at -15 and 0 min before bCRH administration). Mean ACTH concentrations from 0 to 180 min following 0.1 microg of bCRH/kg BW were not significantly different (P = 0.177) from controls. Administration of 0.3, 1.0, and 1.5 microg of bCRH/kg BW increased (P < 0.05) peak ACTH above pretreatment concentrations, and mean ACTH from 0 to 180 min for these treatments were greater (P < 0.05) than for controls. Peak cortisol responses to all bCRH treatments were greater (P < 0.05) than those to pretreatment concentrations. Mean cortisol concentrations from 0 to 180 min were greater (P < 0.05) in all bCRH-treated steers than in controls, but there were no significant differences among the bCRH treatments. The ratio of mean cortisol to mean ACTH for all bCRH doses tested differed (P < 0.05) from control values, indicating reactivity of the adrenals. In conclusion, bCRH challenge may be a useful method for testing the sensitivity of the hypothalamic-pituitary-adrenal axis in steers subjected to stressful husbandry conditions, and a minimum dose of 0.3 microg of bCRH/kg BW is required to stimulate physiological effects of stressor hormones.