This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map 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 KEM, D. C. Articles by HIGGINS, J. R. Search for Related Content PubMed PubMed Citation Articles by KEM, D. C. Articles by HIGGINS, J. R.

Plasma Aldosterone and Renin Activity Response to ACTH Infusion in Dexamethasone-Suppressed Normal and Sodium-Depleted Man

Department of Internal Medicine, University of Texas, Southwestern Medical School Dallas, Texas 75235

Reprint requests to Dr. Kern, room 308D, Department of Internal Medicine University of Oklahoma Health Sciences Center, 800 N.E. 13th Street, Oklahoma City, Oklahoma 73104.

AGTH ±^1–24 was infused at increasing rates of 12.5–200 mIU/30 min in dexamethasone-suppressed normal subjects while on normal and low sodium diets. The lowest infusion rate of ACTH significantly increased the median plasma cortisol concentration from <1.0 µg/100 ml to 3.1 µ/100 ml (p < 0.01) and the median plasma aldosterone concentration from 4.3 ng/100 ml to 8.8 ng/100 ml (p < 0.025) while on a normal sodium diet. Plasma renin activity was not significantly changed during this period. After sodium restriction the peak median plasma aldosterone response to ACTH was 3.8 times that during normal sodium intake while the plasma cortisol response was unchanged. The median plasma renin activity (PRA) rose from 0.45 to 2.45 ng/ml·hr^–1 during the first two infusion periods.

It is estimated from these data that an ACTH infusion rate of 9 mIU/30 min will produce equally significant increases in both plasma cortisol and aldosterone concentrations in such subjects on a regular diet. There was an increased responsiveness of plasma aldosterone to ACTH infusion following sodium restriction which may in part be related to concurrent rises in renin activity. This enhanced response of plasma aldosterone was not totally dependent upon the concurrent rise in PRA since suppression of the latter hormone by infusion of saline failed to abolish the ACTH mediated increase in plasma aldosterone.

Received September 6, 1973.

This article has been cited by other articles:

				J. M. C. Connell, S. M. MacKenzie, E. M. Freel, R. Fraser, and E. Davies A Lifetime of Aldosterone Excess: Long-Term Consequences of Altered Regulation of Aldosterone Production for Cardiovascular Function Endocr. Rev., April 1, 2008; 29(2): 133 - 154. [Abstract] [Full Text] [PDF]

				T. Mancini, B. Kola, F. Mantero, and G. Arnaldi Functional and Nonfunctional Adrenocortical Tumors Demonstrate a High Responsiveness to Low-Dose Adrenocorticotropin J. Clin. Endocrinol. Metab., May 1, 2003; 88(5): 1994 - 1998. [Abstract] [Full Text] [PDF]

				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]

				I. A. Reid Plasma Renin Activity, Aldosterone, and Cortisol Responses To a Short-Acting Intravenous Adrenocorticotropic Hormone Test-Reply Arch Intern Med, May 1, 1986; 146(5): 1021 - 1025. [Abstract] [PDF]

				G. P. Guthrie Jr, E. A. Wilson, D. L. Quillen, and M. J. Jawad Adrenal Androgen Excess and Defective 11{beta}-Hydroxylation in Women With Idiopathic Hirsutism Arch Intern Med, April 1, 1982; 142(4): 729 - 735. [Abstract] [PDF]