| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
The Medical Service, San Francisco General Hospital University of California School of Medicine, San Francisco, California
Address correspondence to: Morris Schambelan, Building 100, Room 321, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, California. Received November 13, 1975.
The effect of circadian rhythm and alterations in posture on plasma aldosterone concentration was studied in 13 patients with primary aldosteronism (six adenoma, five idiopathic hyperplasia, two carcinoma) to define the regulatory mechanism in each of these pathologic subtypes. Blood samples for aldosterone, cortisol, renin, and potassium concentrations were obtained eveiy 4 h during prolonged recumbency (32 h) and upright posture (16 h).
During recumbency, aldosterone and cortisol followed a normal circadian pattern in patients with adenoma and hyperplasia, with peak values at 0400–0800 h and the nadir at 1600–2400 h. Normalized aldosterone and cortisol values correlated significantly in both groups (adenoma r = +0.66, P < 0.001; hyperplasia r = +0.42, P < 0.01). With upright posture, aldosterone levels declined parallel to the normal circadian fall in cortisol in patients with adenoma (r = +0.68, P < 0.001), whereas aldosterone levels increased in patients with hyperplasia parallel to small increments in renin (r = +0.65, P < 0.001) and potassium (r = +0.64, P < 0.001).
During the administration of dexamethasone, aldosterone no longer correlated with cortisol in patients with adenoma but continued to correlate with renin during upright studies in patients with hyperplasia (r = +0.77, P < 0.01). Aldosterone circadian rhythm was abnormal in patients with carcinoma and no effect of posture was noted. Unilateral adrenalectomy restored the normal postural relationship in four patients with adenoma.
These studies suggest that aldosterone secretion is under continuous ACTH control regardless of posture in patients with adenoma, whereas persistent adrenal responsiveness to small increments in renin and/or potassium mediate the postural increase in plasma aldosterone in patients with hyperplasia. True adrenal autonomy occurs only in patients with adrenal carcinoma and when ACTH is suppressed in those with adenoma.
This work was presented at the Annual Meeting of The American Society for Clinical Investigation, Atlantic City, New Jersey, 1975, Clin Res 23: 390A (Abstract).
Received November 13, 1975.
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] |
||||
![]() |
C. E. Fardella, M. Pinto, L. Mosso, C. Gomez-Sanchez, J. Jalil, and J. Montero Genetic Study of Patients with Dexamethasone-Suppressible Aldosteronism without the Chimeric CYP11B1/CYP11B2 Gene J. Clin. Endocrinol. Metab., October 1, 2001; 86(10): 4805 - 4807. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Mosso, C. E. Gomez-Sanchez, M. F. Foecking, and C. Fardella Serum 18-Hydroxycortisol in Primary Aldosteronism, Hypertension, and Normotensives Hypertension, September 1, 2001; 38(3): 688 - 691. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Mulatero, F. Veglio, C. Pilon, F. Rabbia, C. Zocchi, P. Limone, M. Boscaro, N. Sonino, and F. Fallo Diagnosis of Glucocorticoid-Remediable Aldosteronism in Primary Aldosteronism: Aldosterone Response to Dexamethasone and Long Polymerase Chain Reaction for Chimeric Gene J. Clin. Endocrinol. Metab., July 1, 1998; 83(7): 2573 - 2575. [Abstract] [Full Text] |
||||
![]() |
W. R. Litchfield, M. I. New, C. Coolidge, R. P. Lifton, and R. G. Dluhy Evaluation of the Dexamethasone Suppression Test for the Diagnosis of Glucocorticoid-Remediable Aldosteronism J. Clin. Endocrinol. Metab., November 1, 1997; 82(11): 3570 - 3573. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. ARTEAGA, E. G. BIGLIERI, C. E. KATER, J. M. LOPEZ, and M. SCHAMBELAN Aldosterone-Producing Adrenocortical Carcinoma: Preoperative Recognition and Course in Three Cases Ann Intern Med, September 1, 1984; 101(3): 316 - 321. [Abstract] [PDF] |
||||
![]() |
A. Ganguly, C. E. Grim, and M. H. Weinberger Primary Aldosteronism: The Etiologic Spectrum of Disorders and Their Clinical Differentiation Arch Intern Med, April 1, 1982; 142(4): 813 - 815. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |