title: Primary aldosteronism can alter peripheral levels of transforming growth factor beta and tumor necrosis factor alpha.
abstract: Primary aldosteronism (PA) is the most common secondary cause of hypertension that has recently been implicated in alterations of the immune system and progression of cardiovascular disease.
  
  
  OBJECTIVE
  To study the cytokines transforming growth factor beta1 (TGF-beta1), tumor necrosis factor alpha (TNF-alpha), and interleukin 10 (IL-10) in patients with PA and essential hypertensives (EH) and evaluate its association with the renin-angiotensin-aldosterone system.
  
  
  METHODS
  We studied 26 PA and 52 EH patients as controls, adjusted by their blood pressure, body mass index, age, and gender. In both groups, PA and EH, we measured serum aldosterone (SA), plasma renin activity (PRA), and cytokines TGF- beta1, TNF-alpha, and IL-10. In addition, 17 PA patients were treated for 6 months with spironolactone, a mineralocorticoid receptor (MR) antagonist.
  
  
  RESULTS
  PA patients had lower levels of TGF-beta1 (17.6+/-4.1 vs 34.5+/-20.5 pg/ml, p<0.001) and TNF-alpha (17.0+/-4.4 vs 35.6+/-21.7 pg/ml, p<0.001) and similar IL-10 levels (99.7+/-18.7 vs 89.4+/-49.5 pg/ml, p: ns), as compared with EH controls. TGF-beta1 and TNF-alpha levels showed a remarkable correlation with SA/PRA ratio in the total group (PA+EH). The treatment of PA patients with spironolactone increased the TGF-beta1 levels (18.3+/-5.9 to 28.4+/-6.3 pg/ml, p<0.001), while TNF-alpha, and IL-10 remained unchanged.
  
  
  CONCLUSIONS
  Our results showed that PA patients have lower TGF-beta1 and TNF-alpha cytokine serum levels than EH. TGF-beta1 levels were restored with spironolactone, showing a MR-dependent regulation. In this way, the chronic aldosterone excess modifies the TGF-beta1 levels, which could produce an imbalance in the immune system homeostasis that may promote an early proinflammatory cardiovascular phenotype.
authors: Department of Endocrinology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
authors: C A
authors: CA
authors: Carvajal
authors: A A
authors: AA
authors: Herrada
authors: C R
authors: CR
authors: Castillo
authors: F J
authors: FJ
authors: Contreras
authors: C B
authors: CB
authors: Stehr
authors: L M
authors: LM
authors: Mosso
authors: A M
authors: AM
authors: Kalergis
authors: C E
authors: CE
authors: Fardella
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000188:drug therapy / Q000503:physiopathology*; D006973:Hypertension / Q000378:metabolism; D016753:Interleukin-10 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology; D013148:Spironolactone / Q000627:therapeutic use; D016212:Transforming Growth Factor beta / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D013148:Spironolactone; D000450:Aldosterone; D012083:Renin