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J Clin Endocrinol Metab. 2010 Oct;95(10):4756-61. doi: 10.1210/jc.2010-0823. Epub 2010 Jul 21.

Reversible sympathetic overactivity in hypertensive patients with primary aldosteronism.

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  • 1Cardiology Division, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8586, USA.

Abstract

CONTEXT:

Aldosterone has been shown to exert a central sympathoexcitatory action in multiple animal models, but evidence in humans is still lacking.

OBJECTIVES:

Our objective was to determine whether hyperaldosteronism causes reversible sympathetic activation in humans.

METHODS:

We performed a cross-sectional comparison of muscle sympathetic nerve activity (SNA, intraneural microelectrodes) in 14 hypertensive patients with biochemically proven primary aldosteronism (PA) with 20 patients with essential hypertension (EH) and 18 age-matched normotensive (NT) controls. Seven patients with aldosterone-producing adenoma (APA) were restudied 1 month after unilateral adrenalectomy.

RESULTS:

Mean blood pressure values in patients with PA and EH and NT controls was 145 ± 4/88 ± 2, 150 ± 4/90 ± 2, and 119 ± 2/76 ± 2 mm Hg, respectively. The major new findings are 2-fold: 1) baseline SNA was significantly higher in the PA than the NT group (40 ± 3 vs. 30 ± 2 bursts/min, P = 0.014) but similar to the EH group (41 ± 3 bursts/min) and 2) after unilateral adrenalectomy for APA, SNA decreased significantly from 38 ± 5 to 27 ± 4 bursts/min (P = 0.01), plasma aldosterone levels fell from 72.4 ± 20.3 to 11.4 ± 2.3 ng/dl (P < 0.01), and blood pressure decreased from 155 ± 8/94 ± 3 to 117 ± 4/77 ± 2 mm Hg (P < 0.01).

CONCLUSION:

These data provide the first evidence in humans that APA is accompanied by reversible sympathetic overactivity, which may contribute to the accelerated hypertensive target organ disease in this condition.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT00353652.

PMID:
20660053
PMCID:
PMC3050103
DOI:
10.1210/jc.2010-0823
[PubMed - indexed for MEDLINE]
Free PMC Article
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