TY - JOUR
T1 - Reversible sympathetic overactivity in hypertensive patients with primary aldosteronism
AU - Kontak, Andrew C.
AU - Wang, Zhongyun
AU - Arbique, Debbie
AU - Adams-Huet, Beverley
AU - Auchus, Richard J.
AU - Nesbitt, Shawna D.
AU - Victor, Ronald G.
AU - Vongpatanasin, Wanpen
N1 - Funding Information:
This work was supported by National Institutes of Health Grant HL-078782 (W.V.). The project was also supported by the Donald W. Reynold's Cardiovascular Clinical Research Center (R.G.V., W.V.) and the O'Brien Kidney Center (W.V.), the Lincy Foundation (R.G.V.), the Clinical Scientist Award in Translational Research 1005954 from the Burroughs Wellcome Fund (R.A.), and Clinical and Translational Sciences Award UL1RR-024982 (B.A.-H.).
Funding Information:
Disclosure Summary: W.V. is supported by a research grant from the National Institutes of Health ( RO1HL-078782 ). Other authors have nothing to declare.
PY - 2010/10
Y1 - 2010/10
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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U2 - 10.1210/jc.2010-0823
DO - 10.1210/jc.2010-0823
M3 - Article
C2 - 20660053
AN - SCOPUS:77957757456
SN - 0021-972X
VL - 95
SP - 4756
EP - 4761
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 10
ER -