Investigation of the primary cause of hypoadrenocorticism in South African angora goats (Capra aegagrus): a comparison with Boer goats (Capra hircus) and Merino sheep (Ovis aries).
Our objective was to identify the primary site of the reduced adrenal function in South African Angora goats (Capra aegagrus) that causes a decrease in cortisol production and leads to severe losses of Angora goats during cold spells. Angora goats, Boer goats (Capra hircus), and Merino sheep (Ovis aries) were assigned to three intravenous treatments: 1) insulin, 2) corticotropin-releasing factor (CRF), and 3) ACTH. Blood cortisol concentrations were determined over a 90-min period to determine any differences in the response of the experimental animals to these treatments. For both the insulin and ACTH treatments, cortisol concentrations were less in Angora goats than in the other experimental animals. The adrenal gland was subsequently investigated as a possible cause for the observed hypoadrenocorticism. Primary adrenal cell cultures were prepared from these species, subjected to different treatments, and the cortisol production determined. Upon pregnenolone (PREG) addition, all the experimental animals' cortisol production increased significantly, with the production in Boer goats higher (P<.01) when compared with that in the other species. The stimulation of cortisol biosynthesis by ACTH was only obtained for Boer goats and Merino sheep. The stimulation of cortisol production by forskolin and cholera toxin were compared with ACTH, and, for Angora goats, only cholera toxin caused a significant increase in cortisol production. For Boer goats, no difference (P>.05) between the PREG, ACTH, forskolin, or cholera toxin treatments were observed. The Merino adrenal cells were increasingly stimulated in the following order: PREG, ACTH, forskolin, and cholera toxin (forskolin and cholera toxin stimulated cortisol production to the same extent). This investigation of the hypothalamic-pituitary-adrenocortical axis, therefore, identified the adrenal gland as the primary site of the Angora's hypoadrenocorticism.
Engelbrecht
Y
Y
Department of Biochemistry, University of Stellenbosch, South Africa. yebrecht@gerga.sun.ac.za
Herselman
T
T
Louw
A
A
Swart
P
P
D000309:Adrenal Insufficiency / Q000209:etiology / Q000662:veterinary*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D002772:Cholera Toxin / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D005260:Female; D015511:Goat Diseases / Q000209:etiology*; D006041:Goats / Q000145:classification; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D012756:Sheep; D012757:Sheep Diseases / Q000209:etiology*; D013312:Stress, Physiological / Q000097:blood
D005576:Colforsin; D000324:Adrenocorticotropic Hormone; D002772:Cholera Toxin; D003346:Corticotropin-Releasing Hormone; D006854:Hydrocortisone