title: Role of aldosterone in left ventricular hypertrophy in hypertension.
abstract: BACKGROUND
  Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients.
  
  
  METHODS
  A total of 25 patients with primary aldosteronism caused by Conn's adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects.
  
  
  RESULTS
  The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 +/- 7.7, 142.3 +/- 7.2, and 115.2 +/- 7.2 g/m(2), respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism.
  
  
  CONCLUSIONS
  These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan. matsumk@intmed2.med.kyushu-u.ac.jp
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Matsumura
authors.forename: Koji
authors.initials: K
authors.lastname: Fujii
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Oniki
authors.forename: Masayo
authors.initials: M
authors.lastname: Oka
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Iida
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D018246:Adrenocortical Adenoma / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D000328:Adult; D000450:Aldosterone / Q000502:physiology*; D000804:Angiotensin II / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D018660:Blood Pressure Monitoring, Ambulatory; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D004452:Echocardiography; D004719:Endomyocardial Fibrosis / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000150:complications / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000209:etiology / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D000804:Angiotensin II; D000450:Aldosterone