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- Title
Aldosterone Impairs Vascular Smooth Muscle Function: From Clinical to Bench Research.
- Authors
Chou, Chia-Hung; Chen, Ying-Hsien; Hung, Chi-Sheng; Chang, Yi-Yao; Tzeng, Yu-Lin; Wu, Xue-Ming; Wu, Vin-Cent; Tsai, Chia-Ti; Wu, Cho-Kai; Ho, Yi-Lwun; Wu, Kwan-Dun; Lin, Yen-Hung; TAIPAI Study Group
- Abstract
<bold>Context: </bold>The effect of aldosterone on vascular smooth muscle cell function is still unclear. One method to measure vascular smooth muscle cell function is endothelial-independent vascular dilation, for which the key factor is sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA).<bold>Objective: </bold>Our objective was to investigate the effect of aldosterone on vascular smooth muscle cell function and SERCA regulation.<bold>Design: </bold>We prospectively analyzed 35 patients with primary aldosteronism (PA; 32 patients with aldosterone-producing adenoma and three patients with idiopathic hyperaldosteronism) and 30 patients with essential hypertension (EH) who were enrolled as the control group. Flow and nitrate-mediated dilation were performed in both groups and 1 year after adrenalectomy in the patients with aldosterone-producing adenoma. In addition, we investigated the effect of aldosterone on SERCA regulation in human aortic smooth muscle cells.<bold>Setting: </bold>This study took place in an academic clinical research center.<bold>Participants: </bold>Participants included 35 patients with PA and 30 patients with EH.<bold>Interventions: </bold>Adrenalectomy was undertaken in patients with aldosterone-producing adenoma.<bold>Results: </bold>The PA patients had significantly lower flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD) values than the patients with EH (FMD: 13 ± 6 vs 16 ± 4; NMD: 16 ± 6 vs 19 ± 5; both P < .05). FMD/NMD were significantly correlated with log 24 hour-urine aldosterone (FMD: r = -0.287, P = .048; NMD: r = -0.402, P = .005) but not blood pressure. The impaired FMD and NMD values were significantly restored 1 year after adrenalectomy (FMD: 11 ± 4 to 19 ± 7; NMD: 15 ± 6 to 21 ± 6; both P < .01). Under confocal microscopy, aldosterone was shown to suppress the expression of SERCA2a of human aortic smooth muscle cells. Aldosterone significantly suppressed the expression of SERCA2a from 10(-8) M in mRNA and protein levels. This suppression was through down-regulation of mineralocorticoid receptor dependent mitochondrial transcription factors A and B2.<bold>Conclusions: </bold>Aldosterone impairs vascular smooth muscle cell function and suppresses SERCA 2a expression.
- Subjects
ADRENALECTOMY; ALDOSTERONE; BLOOD pressure; VASODILATION; CARRIER proteins; CELL culture; CELL receptors; GENES; HYPERALDOSTERONISM; LONGITUDINAL method; NITRATES; RNA; SMOOTH muscle; TREATMENT effectiveness
- Publication
Journal of Clinical Endocrinology & Metabolism, 2015, Vol 100, Issue 11, p4339
- ISSN
0021-972X
- Publication type
journal article
- DOI
10.1210/jc.2015-2752