(Hypertension. 1999;34:315-319.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Department of Medicine, Indiana University School of Medicine (J.H.P., J.F.R., L.Z., W.T.A., S.A.N.), and VA Medical Center (J.H.P., J.F.R.), Indianapolis, Ind; Harry S. Truman Veterans Hospital (C.E.G.-S.), Columbia, Mo; and Endocrine Sciences (D.F.M.), Calabasas Hills, Calif.
Correspondence to J. Howard Pratt, MD, 541 Clinical Dr, Indianapolis, IN 46202-5111. E-mail johpratt{at}iupui.edu
AbstractBlacks appear, on average, to retain more Na than whites. A higher production rate of mineralocorticoids could explain the greater Na retention in blacks. Although production of aldosterone has been shown to be lower in blacks, the level of another mineralocorticoid may be increased. Plasma levels of deoxycorticosterone and cortisol were measured in young whites (n=23; age=16.4±3.1[SD] years) and young blacks (n=25; age=13.8±1.3 years). Blacks had lower plasma levels of renin activity and aldosterone and lower urinary aldosterone excretion rates; thus, they appeared to be representative of blacks that retain additional Na. Plasma deoxycorticosterone levels were lower in blacks than in whites both at baseline (247±161 versus 381±270 pmol/L, P=0.048) and after stimulation with adrenocorticotropic hormone (822±294 versus 1127±628 pmol/L at 30 minutes, P=0.047; 925±366 versus 1440±834 pmol/L at 60 minutes, P=0.013). Cortisol levels were also lower in blacks at baseline (P=0.014) but were not significantly different from levels in whites after stimulation with adrenocorticotropic hormone. In a larger cohort of 407 whites (age=12.0±2.9 years) and 247 blacks (age=12.9±3.1 years), 18-hydroxycortisol excretion rates were also lower in blacks (P=0.021). In conclusion, increased Na retention in blacks does not appear to be secondary to increased production of either aldosterone, deoxycorticosterone, cortisol, or 18-hydroxycortisol. A primary renal mechanism may mediate the increase in Na reabsorption in blacks.
Key Words: deoxycorticosterone cortisol 18-hydroxycortisol aldosterone race renin
This article has been cited by other articles:
![]() |
C. J. Rodriguez, R. R. Sciacca, A. V. Diez-Roux, B. Boden-Albala, R. L. Sacco, S. Homma, and M. R. DiTullio Relation Between Socioeconomic Status, Race-Ethnicity, and Left Ventricular Mass: The Northern Manhattan Study Hypertension, April 1, 2004; 43(4): 775 - 779. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. K Shieh, E. Kotlyar, and F. Sam Aldosterone and cardiovascular remodelling: focus on myocardial failure Journal of Renin-Angiotensin-Aldosterone System, March 1, 2004; 5(1): 3 - 13. [Abstract] [PDF] |
||||
![]() |
C. Winter, N. Schulz, G. Giebisch, J. P. Geibel, and C. A. Wagner Nongenomic stimulation of vacuolar H+-ATPases in intercalated renal tubule cells by aldosterone PNAS, February 24, 2004; 101(8): 2636 - 2641. [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] |
||||
![]() |
A. H. El-Gharbawy, V. S. Nadig, J. M. Kotchen, C. E. Grim, K. B. Sagar, M. Kaldunski, P. Hamet, Z. Pausova, D. Gaudet, F. Gossard, et al. Arterial Pressure, Left Ventricular Mass, and Aldosterone in Essential Hypertension Hypertension, March 1, 2001; 37(3): 845 - 850. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. T. Ambrosius, L. J. Bloem, L. Zhou, J. F. Rebhun, P. M. Snyder, M. A. Wagner, C. Guo, and J. H. Pratt Genetic Variants in the Epithelial Sodium Channel in Relation to Aldosterone and Potassium Excretion and Risk for Hypertension Hypertension, October 1, 1999; 34(4): 631 - 637. [Abstract] [Full Text] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1999 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |