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(Hypertension. 2005;46:469.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Improvement of Blood Pressure With Inhibition of the Epithelial Sodium Channel in Blacks With Hypertension

David G. Warnock; P. Darwin Bell

From the Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham.

Correspondence to David G. Warnock, MD, Room 647 THT, 1530 Third Ave S, UAB Station, Birmingham, AL 35294-0006. E-mail dwarnock@uab.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The epithelial sodium channel (ENaC) is a critically important final regulator of the balance between intake and excretion of dietary sodium,¹ and along with the thiazide-sensitive NaCl cotransporter, constitutes the predominant sodium transport systems in the aldosterone-sensitive distal nephron.² As proposed by Guyton,³ and confirmed by the unraveling of the activating ENaC mutations in Liddle’s syndrome,⁴ dysregulation of the final balance of sodium intake and excretion can result in chronic volume expansion, plasma renin suppression, and arterial hypertension.¹ Blacks often have low-renin, salt-sensitive hypertension, which could be explained by some sort of persisting activation of ENaC, even in the face of relative excess dietary salt intake.⁵ The possibility that polymorphisms in the 3 ENaC subunits could contribute to this apparent activation of ENaC⁶ and the utility of amiloride as an ENaC blocker in black hypertension have been considered previously.⁷

In this issue of journal, Saha et al⁸ describe a systematic investigation of the effects of amiloride, spironolactone, and their use in combination in a short-term, randomized, placebo-controlled crossover study in blacks with established low-renin hypertension. As such, these studies represent important extension of the previous work of this group published in Hypertension.⁹ Both agents block the effects of aldosterone on the aldosterone-sensitive distal nephron, with amiloride directly interacting with ENaC and spironolactone affecting all aldosterone-sensitive systems, including ENaC and the thiazide-sensitive NaCl cotransporter.² Of note, the 98 black subjects in this report were hypertensive despite treatment that included thiazides and calcium channel blockers. Amiloride and spironolactone significantly reduced systolic . . . [Full Text of this Article]

Related Article:

Improvement in Blood Pressure With Inhibition of the Epithelial Sodium Channel in Blacks With Hypertension

Chandan Saha, George J. Eckert, Walter T. Ambrosius, Tae-Yon Chun, Mary Anne Wagner, Qianqian Zhao, and J. Howard Pratt
Hypertension 2005 46: 481-487. [Abstract] [Full Text] [PDF]