This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by SIRETT, N. E. Articles by GIBBS, F. P. Search for Related Content PubMed PubMed Citation Articles by SIRETT, N. E. Articles by GIBBS, F. P.

Dexamethasone Suppression of ACTH Release: Effect of the Interval Between Steroid Administration and the Application of Stimuli Known To Release ACTH

Division of Endocrinology, Department of Medicine, University of Oregon Medical School Portland, Oregon 97201

Abstract

Dexamethasone was given to female rats by intraperitoneal injection (400 µg/100 g) or in the overnight drinking water (20 µg/ml). ACTH release was studied by measuring the plasma corticosterone response 20 min after the application of various stimuli. Four hr after the injection of dexamethasone the response to a tourniquet about the calf was inhibited; the response to urethane, gut stretch, hemorrhage or 50 mU/100 g vasopressin was partially inhibited but there was no inhibition of the response to 500 mU/100 g vasopressin. Overnight dexamethasone markedly reduced the response to all stimuli except 500 mil vasopressin. The relationship between the time of injection of dexamethasone and the application of the stimulus was tested by stimulating ACTH release with ip urethane. Ten hr after injection of dexamethasone there was complete suppression of ACTH release in response to urethane, but this suppression largely disappeared at 24 hr. It is concluded that the inhibition of ACTH release by large doses of dexamethasone is a function of the strength of the ACTH-releasing stimulus and the time interval between the administration of the dexamethasone and the application of the stimulus. (Endocrinology 85: 355, 1969)

Footnotes

Received August 29, 1968. Supported by Grants AM-01447, AM-08547 and AM-05065 from the National Institute of Arthritis and Metabolic Diseases, NIH, USPHS.

¹ Visiting Scientist. Present address: Medical Research Council of New Zealand, Endocrinology Research Department, Medical School, Box 913, Dunedin, New Zealand.

² Trainee in Endocrinology. Present address: Department of Anatomy, University of Rochester, School of Medicine and Dentistry, Rochester, N. Y. 14620.

Received August 29, 1968.

This article has been cited by other articles:

				D. M. Roesch, Y. Tian, W. Zheng, M. Shi, J. G. Verbalis, and K. Sandberg Estradiol Attenuates Angiotensin-Induced Aldosterone Secretion in Ovariectomized Rats Endocrinology, December 1, 2000; 141(12): 4629 - 4636. [Abstract] [Full Text] [PDF]

				D. M Roesch, Ying Tian, J. G Verbalis, and K. Sandberg Rat model for investigating ACTH-independent angiotensin-induced aldosterone secretion Journal of Renin-Angiotensin-Aldosterone System, March 1, 2000; 1(1): 36 - 39. [Abstract] [PDF]