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(Hypertension. 1999;34:395-397.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Division of Nephrology, University of Alabama at Birmingham.
Correspondence to David G, Warnock, MD, Professor of Medicine and Physiology Director, Division of Nephrology, University of Alabama at Birmingham, 647 Tinsley Harrison Tower, 1900 University Blvd, Birmingham, AL 35294-0007. E-mail dwarnock@nrtc.dom.uab.edu
Key Words: blacks renin aldosterone endothelial sodium channel Liddle's syndrome
| Introduction |
|---|
Studies by Fisher et al2 focus on adrenal and
pressor responsiveness to angiotensin II (Ang II) as
a function of dietary salt intake in patients with LREH, normal-renin
hypertension, and normal controls. Especially striking are the
functional similarities between LREH and " nonmodulating" essential
hypertension with normal plasma renin activity (NMEH), including: (1)
salt-sensitivity of the blood pressure; (2) blunted plasma
aldosterone responses to Ang II infusion and upright
posture after 5 days of rigid dietary sodium restriction; and (3)
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