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Department of Endocrinology, The Princess Margaret Hospital Christchurch 2, New Zealand;
Peptide Biology Laboratory, The Salk Institute for Biological Studies La Jolla, California 92037
Address requests for reprints to: Dr. R. A. Donald, Department of Endocrinology, The Princess Margaret Hospital, Christchurch 2, New Zealand.
Abstract
The 41-residue ovine corticotropin releasing factor (CRF) was administered iv and intracerebroventricularly (icv) to merino sheep. A significant rise in plasma ACTH, β- lipotropin (βLPH) and cortisol was demonstrated after the administration of 200 µg, iv. A highly significant correlation between the increments in plasma ACTH and βLPH was observed. The plasma ACTH rise was evident within 5 min and was abolished by the prior administration of 0.4–4.0 mg dexamethasone. No significant rise in plasma GH, LH, PRL, insulin, glucagon, pancreatic polypeptide, met-enkephalin, angiotensin II, aldosterone, or vasopressin could be demonstrated. Although smaller doses of CRF (50 ng to 5 µg) were effective when given icv, the ACTH response was more delayed.
It is concluded that CRF stimulates a rapid increase in the secretion of ACTH and βLPH in sheep. Suppression of this response by dexamethasone indicates that glucocorticoids are capable of acting on the pituitary to inhibit the ACTH response to CRF. The delayed response when CRF is given icv may be due to diffusion. The action of CRF appears to be relatively specific, in that the plasma concentrations of the other pancreatic, pituitary, and adrenal hormones measured were not affected. (Endocrinology 113: 866,1983)
Footnotes
* This work was supported by a grant from the New Zealand Medical Research Council and NIH Grant AM-26741-01.
Received September 27, 1982.
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