HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by van Wijk, P. A Articles by Mol, J. A Search for Related Content PubMed Articles by van Wijk, P. A Articles by Mol, J. A

Responsiveness to corticotropin-releasing hormone and vasopressin in canine Cushing's syndrome

Van Wijk PA, Rijnberk A, Croughs RJM, Wolfswinkel J, Selman PJ, Mol JA. Responsiveness to corticotropin-releasing hormone and vasopressin in canine Cushing's syndrome. Eur J Endocrinol 1994;130:410–16. ISSN 0804–4643

Corticotropin-releasing hormone (CRH) and vasopressin are the most important hypothalamic factors regulating adrenocorticotropic hormone (ACTH) secretion. In this study we have investigated the responsiveness of the pituitary–adrenocortical axis to intravenous administration of CRH or lysine vasopressin (LVP) in 16 control dogs, 22 dogs with pituitary-dependent hyperadrenocorticism and five dogs with hyperadrenocorticism due to an adrenocortical tumor, using doses of CRH and LVP that caused equivalent ACTH responses in the control dogs. After CRH administration, the increment in plasma ACTH was significantly (p < 0.05) lower in dogs with pituitary-dependent hyperadrenocorticism (221 ± 53 ng/l) than that in control dogs (279 ± ng/l). In the dogs with pituitary-dependent hyperadrenocorticism, the relative increases in ACTH after CRH were significantly (p < 0.05) lower than those after LVP. Despite the absence of an increase in ACTH following LVP administration in dogs with hyperadrenocorticism due to an adrenocortical tumor, there was a significant increase in plasma cortisol, the increment (790 ±238 nmol/l) being not statistically different from that in the control dogs (412 ± 37 nmol/l). We conclude that in spite of the changes inherent to pituitary-dependent hyperadrenocorticism, i.e. neoplastic transformation of corticotropic cells and hypercortisolism, there is persistence of responsiveness to hypophysiotropic hormones. The ACTH secretion by corticotropic cells in pituitary-dependent hyperadrenocorticism was relatively less sensitive to stimulation with CRH than with LVP. Adrenocortical tumors develop an aberrant sensitivity to LVP.

A Rijnberk, Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, PO Box 80.154, 3508 TD, Utrecht, The Netherlands

This article has been cited by other articles:

				A. Lacroix, N. N'Diaye, J. Tremblay, and P. Hamet Ectopic and Abnormal Hormone Receptors in Adrenal Cushing's Syndrome Endocr. Rev., February 1, 2001; 22(1): 75 - 110. [Abstract] [Full Text]

				G. Arnaldi, J.-M. Gasc, Y. de Keyzer, M.-L. Raffin-Sanson, V. Perraudin, J.-M. Kuhn, M.-C. Raux-Demay, J.-P. Luton, E. Clauser, and X. Bertagna Variable Expression of the V1 Vasopressin Receptor Modulates the Phenotypic Response of Steroid-Secreting Adrenocortical Tumors J. Clin. Endocrinol. Metab., June 1, 1998; 83(6): 2029 - 2035. [Abstract] [Full Text]

				A. Lacroix, J. Tremblay, R. M. Touyz, L. Y. Deng, R. Lariviere, J. R. Cusson, E. L. Schiffrin, and P. Hamet Abnormal Adrenal and Vascular Responses to Vasopressin Mediated by a V1-Vasopressin Receptor in a Patient with Adrenocorticotropin-Independent Macronodular Adrenal Hyperplasia, Cushing's Syndrome, and Orthostatic Hypotension J. Clin. Endocrinol. Metab., August 1, 1997; 82(8): 2414 - 2422. [Abstract] [Full Text] [PDF]