Role of aldosterone in left ventricular hypertrophy in hypertension

Kiyoshi Matsumura, Koji Fujii, Hideyuki Oniki, Masayo Oka, Mitsuo Iida

研究成果: ジャーナルへの寄稿記事

79 引用 (Scopus)

抄録

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/m2, 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.

元の言語英語
ページ(範囲)13-18
ページ数6
ジャーナルAmerican Journal of Hypertension
19
発行部数1
DOI
出版物ステータス出版済み - 1 1 2006

Fingerprint

Left Ventricular Hypertrophy
Aldosterone
Hypertension
Renovascular Hypertension
Hyperaldosteronism
Blood Pressure
Hypertensive Retinopathy
Adrenocortical Adenoma
Ambulatory Blood Pressure Monitoring
Proteinuria
Angiotensin II
Body Mass Index
Fibrosis
Animal Models
Heart Rate
Essential Hypertension

All Science Journal Classification (ASJC) codes

  • Internal Medicine

これを引用

Role of aldosterone in left ventricular hypertrophy in hypertension. / Matsumura, Kiyoshi; Fujii, Koji; Oniki, Hideyuki; Oka, Masayo; Iida, Mitsuo.

:: American Journal of Hypertension, 巻 19, 番号 1, 01.01.2006, p. 13-18.

研究成果: ジャーナルへの寄稿記事

Matsumura, Kiyoshi ; Fujii, Koji ; Oniki, Hideyuki ; Oka, Masayo ; Iida, Mitsuo. / Role of aldosterone in left ventricular hypertrophy in hypertension. :: American Journal of Hypertension. 2006 ; 巻 19, 番号 1. pp. 13-18.
@article{1eb9e14daf7e47e792d7d57bea1d3986,
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/m2, 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.",
author = "Kiyoshi Matsumura and Koji Fujii and Hideyuki Oniki and Masayo Oka and Mitsuo Iida",
year = "2006",
month = "1",
day = "1",
doi = "10.1016/j.amjhyper.2005.05.013",
language = "English",
volume = "19",
pages = "13--18",
journal = "American Journal of Hypertension",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "1",

}

TY - JOUR

T1 - Role of aldosterone in left ventricular hypertrophy in hypertension

AU - Matsumura, Kiyoshi

AU - Fujii, Koji

AU - Oniki, Hideyuki

AU - Oka, Masayo

AU - Iida, Mitsuo

PY - 2006/1/1

Y1 - 2006/1/1

N2 - 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/m2, 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.

AB - 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/m2, 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.

UR - http://www.scopus.com/inward/record.url?scp=32344443557&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=32344443557&partnerID=8YFLogxK

U2 - 10.1016/j.amjhyper.2005.05.013

DO - 10.1016/j.amjhyper.2005.05.013

M3 - Article

C2 - 16461184

AN - SCOPUS:32344443557

VL - 19

SP - 13

EP - 18

JO - American Journal of Hypertension

JF - American Journal of Hypertension

SN - 0895-7061

IS - 1

ER -