| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Journal of Clinical Endocrinology & Metabolism, Vol 44, 799-802, Copyright © 1977 by Endocrine Society
ARTICLES |
S Ulick, LC Ramirez and MI New
Studies in a juvenile hypertensive syndrome associated with suppressed plasma renin activity and hypokalemic alkalosis failed to reveal overproduction of aldosterone or any other known steroid. There was however an abnormal increase in the fraction of unconjugated urinary steroids. Analysis of this fraction following the administration of labeled cortisol revealed that it was largely composed of dihydro metabolites reduced either at 4,5 or at C-20 and that the 4,5-dihydro fraction contained an abnormal increase in 5alpha- relative to 5beta- metabolites. There was, however, no absolute defect in the complete reduction of ring A to form tetrahydro derivatives. These findings, together with observations by Marver and Edelman that 5alpha- dihydrocortisol may be an effective mineralcorticoid, suggest the possibility of an etiologic relationship between the metabolic abnormality and the patient's hypertensive disorder.
This article has been cited by other articles:
![]() |
P. Strazzullo, F. Galletti, and G. Barba Altered Renal Handling of Sodium in Human Hypertension: Short Review of the Evidence Hypertension, May 1, 2003; 41(5): 1000 - 1005. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. I. New and R. C. Wilson Steroid disorders in children: Congenital adrenal hyperplasia and apparent mineralocorticoid excess PNAS, October 26, 1999; 96(22): 12790 - 12797. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Morineau, J.-M. Marc, A. Boudi, H. Galons, M. Gourmelen, P. Corvol, L. Pascoe, and J. Fiet Genetic, Biochemical, and Clinical Studies of Patients With A328V or R213C Mutations in 11{beta}HSD2 Causing Apparent Mineralocorticoid Excess Hypertension, September 1, 1999; 34(3): 435 - 441. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. C. Wilson, S. Dave-Sharma, J.-Q. Wei, V. R. Obeyesekere, K. Li, P. Ferrari, Z. S. Krozowski, C. H. L. Shackleton, L. Bradlow, T. Wiens, et al. A genetic defect resulting in mild low-renin hypertension PNAS, August 18, 1998; 95(17): 10200 - 10205. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Dave-Sharma, R. C. Wilson, M. D. Harbison, R. Newfield, M. R. Azar, Z. S. Krozowski, J. W. Funder, C. H. L. Shackleton, H. L. Bradlow, J.-Q. Wei, et al. Examination of Genotype and Phenotype Relationships in 14 Patients with Apparent Mineralocorticoid Excess J. Clin. Endocrinol. Metab., July 1, 1998; 83(7): 2244 - 2254. [Abstract] [Full Text] |
||||
![]() |
D. J. Morris, S. A. Latif, M. D. Rokaw, C. O. Watlington, and J. P. Johnson A second enzyme protecting mineralocorticoid receptors from glucocorticoid occupancy Am J Physiol Cell Physiol, May 1, 1998; 274(5): C1245 - C1252. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. V. Mericq and G. B. Cutler Jr. High Fluid Intake Increases Urine Free Cortisol Excretion in Normal Subjects J. Clin. Endocrinol. Metab., February 1, 1998; 83(2): 682 - 684. [Abstract] [Full Text] |
||||
![]() |
G. Morineau, A. Boudi, A. Barka, M. Gourmelen, F. Degeilh, N. Hardy, A. Al-Halnak, H. Soliman, J. P. Gosling, R. Julien, et al. Radioimmunoassay of cortisone in serum, urine, and saliva to assess the status of the cortisol–cortisone shuttle Clin. Chem., August 1, 1997; 43(8): 1397 - 1407. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Morineau, J. Gosling, M.-C. Patricot, H. Soliman, P. Boudou, A. A. Halnak, G. Le Brun, J.-L. Brerault, R. Julien, J.-M. Villette, et al. Convenient chromatographic prepurification step before measurement of urinary cortisol by radioimmunoassay Clin. Chem., May 1, 1997; 43(5): 786 - 793. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. C. White, T. Mune, and A. K. Agarwal 11{beta}-Hydroxysteroid Dehydrogenase and the Syndrome of Apparent Mineralocorticoid Excess Endocr. Rev., February 1, 1997; 18(1): 135 - 156. [Abstract] [Full Text] |
||||
![]() |
G. W. Souness and D. J. Morris 11{alpha}- and 11ß-Hydroxyprogesterone, Potent Inhibitors of 11ß-Hydroxysteroid Dehydrogenase, Possess Hypertensinogenic Activity in the Rat Hypertension, March 1, 1996; 27(3): 421 - 425. [Abstract] [Full Text] |
||||
![]() |
A. Soro, M. C. Ingram, G. Tonolo, N. Glorioso, and R. Fraser Evidence of Coexisting Changes in 11ß-Hydroxysteroid Dehydrogenase and 5ß-Reductase Activity in Subjects With Untreated Essential Hypertension Hypertension, January 1, 1995; 25(1): 67 - 70. [Abstract] [Full Text] |
||||
![]() |
J. Funder, P. Pearce, R Smith, and A. Smith Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated Science, October 28, 1988; 242(4878): 583 - 585. [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 |