Reversible sympathetic overactivity in hypertensive patients with primary aldosteronism

Andrew C. Kontak, Zhongyun Wang, Debbie Arbique, Beverley Adams-Huet, Richard J. Auchus, Shawna D. Nesbitt, Ronald G. Victor, Wanpen Vongpatanasin

Research output: Contribution to journalArticle

44 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)4756-4761
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume95
Issue number10
DOIs
StatePublished - Oct 2010

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Hyperaldosteronism
Aldosterone
Adenoma
Adrenalectomy
Blood pressure
Blood Pressure
Microelectrodes
Muscle
Animals
Animal Models
Chemical activation
Plasmas
Muscles
Essential Hypertension

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Endocrinology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

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Reversible sympathetic overactivity in hypertensive patients with primary aldosteronism. / Kontak, Andrew C.; Wang, Zhongyun; Arbique, Debbie; Adams-Huet, Beverley; Auchus, Richard J.; Nesbitt, Shawna D.; Victor, Ronald G.; Vongpatanasin, Wanpen.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 95, No. 10, 10.2010, p. 4756-4761.

Research output: Contribution to journalArticle

Kontak, Andrew C. ; Wang, Zhongyun ; Arbique, Debbie ; Adams-Huet, Beverley ; Auchus, Richard J. ; Nesbitt, Shawna D. ; Victor, Ronald G. ; Vongpatanasin, Wanpen. / Reversible sympathetic overactivity in hypertensive patients with primary aldosteronism. In: Journal of Clinical Endocrinology and Metabolism. 2010 ; Vol. 95, No. 10. pp. 4756-4761.
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AU - Auchus, Richard J.

AU - Nesbitt, Shawna D.

AU - Victor, Ronald G.

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N2 - 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.

AB - 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.

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