Effects of synthetic ovine corticotropin-releasing hormone on plasma concentrations of immunoreactive adrenocorticotropin, alpha-melanocyte-stimulating hormone, and cortisol in dogs with naturally acquired adrenocortical insufficiency

Mark E. Peterson From The Animal Medical Center and Cornell University Medical College, New York, NY 10021 (Peterson), College of Veterinary Medicine, Auburn University, AL 36849 (Kemppainen), and Vanderbilt University, Medical Center, Nashville, TN 37232 (Orth).

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Robert J. Kemppainen From The Animal Medical Center and Cornell University Medical College, New York, NY 10021 (Peterson), College of Veterinary Medicine, Auburn University, AL 36849 (Kemppainen), and Vanderbilt University, Medical Center, Nashville, TN 37232 (Orth).

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David N. Orth From The Animal Medical Center and Cornell University Medical College, New York, NY 10021 (Peterson), College of Veterinary Medicine, Auburn University, AL 36849 (Kemppainen), and Vanderbilt University, Medical Center, Nashville, TN 37232 (Orth).

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Summary

We evaluated the effect of ovine corticotropin-releasing hormone (crh) on plasma immunoreactive (ir) concentrations of acth, α-melanocyte-stimulating hormone, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma ir-acth concentrations and exaggerated acth responses to crh administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal ir-acth concentrations and a nearly normal response to crh. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma ir-acth concentrations, which failed to increase after administration of crh. Basal plasma α-melanocyte-stimulating hormone concentrations in the dogs with adrenal insufficiency were within normal range and were unaffected by crh administration. In all 8 dogs with adrenal insufficiency, plasma cortisol concentrations were low and did not increase after administration of crh. Therefore, stimulation with crh produced 2 patterns of plasma ir-acth response when administered to dogs with naturally acquired adrenal insufficiency. Dogs with primary adrenal insufficiency had high basal plasma ir-acth concentrations and exaggerated responses to crh, whereas the dog with secondary adrenal insufficiency had undetectable basal plasma concentrations of ir-acth that did not increase after stimulation with crh.

Summary

We evaluated the effect of ovine corticotropin-releasing hormone (crh) on plasma immunoreactive (ir) concentrations of acth, α-melanocyte-stimulating hormone, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma ir-acth concentrations and exaggerated acth responses to crh administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal ir-acth concentrations and a nearly normal response to crh. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma ir-acth concentrations, which failed to increase after administration of crh. Basal plasma α-melanocyte-stimulating hormone concentrations in the dogs with adrenal insufficiency were within normal range and were unaffected by crh administration. In all 8 dogs with adrenal insufficiency, plasma cortisol concentrations were low and did not increase after administration of crh. Therefore, stimulation with crh produced 2 patterns of plasma ir-acth response when administered to dogs with naturally acquired adrenal insufficiency. Dogs with primary adrenal insufficiency had high basal plasma ir-acth concentrations and exaggerated responses to crh, whereas the dog with secondary adrenal insufficiency had undetectable basal plasma concentrations of ir-acth that did not increase after stimulation with crh.

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