Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin

Tae Hwa Chun, Hiroshi Itoh, Takatoshi Saito, Ken Ichi Yamahara, Kentaro Doi, Yuko Mori, Yoshihiro Ogawa, Jun Yamashita, Tokuji Tanaka, Mayumi Inoue, Ken Masatsugu, Naoki Sawada, Yasutomo Fukunaga, Kazuwa Nakao

研究成果: Article

73 引用 (Scopus)

抄録

Objective. Excess oxidative stress is one of the major metabolic abnormalities on vascular walls in hypertension and atherosclerosis. In order to further elucidate the endothelial function under oxidative stress, the effect of hydrogen peroxide (H2O2) on expression of two novel endothelium-derived vasorelaxing peptides, C-type natriuretic peptide (CNP) and adrenomedullin (AM) from bovine carotid artery endothelial cells (BCAECs) was examined. Methods. BCAECs were treated with H2O2 (0.1-1.0 mmol/l) and/or an antioxidant, N-acetylcysteine (NAC) (5-10 mmol/l), and incubated for 48 h. The concentrations of CNP and AM were measured with the specific radioimmunassays that we originally developed. CNP and AM mRNA expressions were also examined by reverse transcription-polymerase chain reaction (RT-PCR). Results. Treatment of BCAECs with 0.5 and 1 mmol/l H2O2 induced 9- and 10-fold increases of CNP concentration in the media. Addition of 10 mmol/l NAC significantly suppressed the effect of H2O2 by 52%. RT-PCR analysis showed that CNP mRNA expression in BCAECs was also rapidly augmented within 1 h with H2O2 (1 mmol/l) treatment, and reached a peak at 3 h to show a 10-fold increase. AM secretion from BCAECs also increased to two-fold with exposure to 0.5 mmol/l H2O2, accompanied with the augmented level of AM mRNA. NAC 10 mmol/l completely suppressed the effect of H2O2 on AM secretion. Conclusions. In this study, it has been demonstrated that H2O2 augments endothelial secretion of the two endothelium-derived relaxing peptides, CNP and AM. Our findings suggest the increased secretion of CNP and AM from endothelium under oxidative stress may function to compensate the impaired nitric oxide-dependent vasorelaxation in hypertension and atherosclerosis. (C) Lippincott Williams and Wilkins.

元の言語English
ページ(範囲)575-580
ページ数6
ジャーナルJournal of Hypertension
18
発行部数5
出版物ステータスPublished - 2000
外部発表Yes

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C-Type Natriuretic Peptide
Adrenomedullin
Endothelium
Oxidative Stress
Carotid Arteries
Endothelial Cells
Acetylcysteine
Messenger RNA
Reverse Transcription
Atherosclerosis
Hypertension
Polymerase Chain Reaction
polypeptide C
Vasodilation
Hydrogen Peroxide
Blood Vessels
Nitric Oxide
Antioxidants

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

これを引用

Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin. / Chun, Tae Hwa; Itoh, Hiroshi; Saito, Takatoshi; Yamahara, Ken Ichi; Doi, Kentaro; Mori, Yuko; Ogawa, Yoshihiro; Yamashita, Jun; Tanaka, Tokuji; Inoue, Mayumi; Masatsugu, Ken; Sawada, Naoki; Fukunaga, Yasutomo; Nakao, Kazuwa.

:: Journal of Hypertension, 巻 18, 番号 5, 2000, p. 575-580.

研究成果: Article

Chun, TH, Itoh, H, Saito, T, Yamahara, KI, Doi, K, Mori, Y, Ogawa, Y, Yamashita, J, Tanaka, T, Inoue, M, Masatsugu, K, Sawada, N, Fukunaga, Y & Nakao, K 2000, 'Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin', Journal of Hypertension, 巻. 18, 番号 5, pp. 575-580.
Chun, Tae Hwa ; Itoh, Hiroshi ; Saito, Takatoshi ; Yamahara, Ken Ichi ; Doi, Kentaro ; Mori, Yuko ; Ogawa, Yoshihiro ; Yamashita, Jun ; Tanaka, Tokuji ; Inoue, Mayumi ; Masatsugu, Ken ; Sawada, Naoki ; Fukunaga, Yasutomo ; Nakao, Kazuwa. / Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin. :: Journal of Hypertension. 2000 ; 巻 18, 番号 5. pp. 575-580.
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title = "Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin",
abstract = "Objective. Excess oxidative stress is one of the major metabolic abnormalities on vascular walls in hypertension and atherosclerosis. In order to further elucidate the endothelial function under oxidative stress, the effect of hydrogen peroxide (H2O2) on expression of two novel endothelium-derived vasorelaxing peptides, C-type natriuretic peptide (CNP) and adrenomedullin (AM) from bovine carotid artery endothelial cells (BCAECs) was examined. Methods. BCAECs were treated with H2O2 (0.1-1.0 mmol/l) and/or an antioxidant, N-acetylcysteine (NAC) (5-10 mmol/l), and incubated for 48 h. The concentrations of CNP and AM were measured with the specific radioimmunassays that we originally developed. CNP and AM mRNA expressions were also examined by reverse transcription-polymerase chain reaction (RT-PCR). Results. Treatment of BCAECs with 0.5 and 1 mmol/l H2O2 induced 9- and 10-fold increases of CNP concentration in the media. Addition of 10 mmol/l NAC significantly suppressed the effect of H2O2 by 52{\%}. RT-PCR analysis showed that CNP mRNA expression in BCAECs was also rapidly augmented within 1 h with H2O2 (1 mmol/l) treatment, and reached a peak at 3 h to show a 10-fold increase. AM secretion from BCAECs also increased to two-fold with exposure to 0.5 mmol/l H2O2, accompanied with the augmented level of AM mRNA. NAC 10 mmol/l completely suppressed the effect of H2O2 on AM secretion. Conclusions. In this study, it has been demonstrated that H2O2 augments endothelial secretion of the two endothelium-derived relaxing peptides, CNP and AM. Our findings suggest the increased secretion of CNP and AM from endothelium under oxidative stress may function to compensate the impaired nitric oxide-dependent vasorelaxation in hypertension and atherosclerosis. (C) Lippincott Williams and Wilkins.",
keywords = "Adrenomedullin, Endothelial cells, Hydrogen peroxide, N-acetylcysteine, Natriuretic peptide, Oxidative stress",
author = "Chun, {Tae Hwa} and Hiroshi Itoh and Takatoshi Saito and Yamahara, {Ken Ichi} and Kentaro Doi and Yuko Mori and Yoshihiro Ogawa and Jun Yamashita and Tokuji Tanaka and Mayumi Inoue and Ken Masatsugu and Naoki Sawada and Yasutomo Fukunaga and Kazuwa Nakao",
year = "2000",
language = "English",
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pages = "575--580",
journal = "Journal of Hypertension",
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}

TY - JOUR

T1 - Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin

AU - Chun, Tae Hwa

AU - Itoh, Hiroshi

AU - Saito, Takatoshi

AU - Yamahara, Ken Ichi

AU - Doi, Kentaro

AU - Mori, Yuko

AU - Ogawa, Yoshihiro

AU - Yamashita, Jun

AU - Tanaka, Tokuji

AU - Inoue, Mayumi

AU - Masatsugu, Ken

AU - Sawada, Naoki

AU - Fukunaga, Yasutomo

AU - Nakao, Kazuwa

PY - 2000

Y1 - 2000

N2 - Objective. Excess oxidative stress is one of the major metabolic abnormalities on vascular walls in hypertension and atherosclerosis. In order to further elucidate the endothelial function under oxidative stress, the effect of hydrogen peroxide (H2O2) on expression of two novel endothelium-derived vasorelaxing peptides, C-type natriuretic peptide (CNP) and adrenomedullin (AM) from bovine carotid artery endothelial cells (BCAECs) was examined. Methods. BCAECs were treated with H2O2 (0.1-1.0 mmol/l) and/or an antioxidant, N-acetylcysteine (NAC) (5-10 mmol/l), and incubated for 48 h. The concentrations of CNP and AM were measured with the specific radioimmunassays that we originally developed. CNP and AM mRNA expressions were also examined by reverse transcription-polymerase chain reaction (RT-PCR). Results. Treatment of BCAECs with 0.5 and 1 mmol/l H2O2 induced 9- and 10-fold increases of CNP concentration in the media. Addition of 10 mmol/l NAC significantly suppressed the effect of H2O2 by 52%. RT-PCR analysis showed that CNP mRNA expression in BCAECs was also rapidly augmented within 1 h with H2O2 (1 mmol/l) treatment, and reached a peak at 3 h to show a 10-fold increase. AM secretion from BCAECs also increased to two-fold with exposure to 0.5 mmol/l H2O2, accompanied with the augmented level of AM mRNA. NAC 10 mmol/l completely suppressed the effect of H2O2 on AM secretion. Conclusions. In this study, it has been demonstrated that H2O2 augments endothelial secretion of the two endothelium-derived relaxing peptides, CNP and AM. Our findings suggest the increased secretion of CNP and AM from endothelium under oxidative stress may function to compensate the impaired nitric oxide-dependent vasorelaxation in hypertension and atherosclerosis. (C) Lippincott Williams and Wilkins.

AB - Objective. Excess oxidative stress is one of the major metabolic abnormalities on vascular walls in hypertension and atherosclerosis. In order to further elucidate the endothelial function under oxidative stress, the effect of hydrogen peroxide (H2O2) on expression of two novel endothelium-derived vasorelaxing peptides, C-type natriuretic peptide (CNP) and adrenomedullin (AM) from bovine carotid artery endothelial cells (BCAECs) was examined. Methods. BCAECs were treated with H2O2 (0.1-1.0 mmol/l) and/or an antioxidant, N-acetylcysteine (NAC) (5-10 mmol/l), and incubated for 48 h. The concentrations of CNP and AM were measured with the specific radioimmunassays that we originally developed. CNP and AM mRNA expressions were also examined by reverse transcription-polymerase chain reaction (RT-PCR). Results. Treatment of BCAECs with 0.5 and 1 mmol/l H2O2 induced 9- and 10-fold increases of CNP concentration in the media. Addition of 10 mmol/l NAC significantly suppressed the effect of H2O2 by 52%. RT-PCR analysis showed that CNP mRNA expression in BCAECs was also rapidly augmented within 1 h with H2O2 (1 mmol/l) treatment, and reached a peak at 3 h to show a 10-fold increase. AM secretion from BCAECs also increased to two-fold with exposure to 0.5 mmol/l H2O2, accompanied with the augmented level of AM mRNA. NAC 10 mmol/l completely suppressed the effect of H2O2 on AM secretion. Conclusions. In this study, it has been demonstrated that H2O2 augments endothelial secretion of the two endothelium-derived relaxing peptides, CNP and AM. Our findings suggest the increased secretion of CNP and AM from endothelium under oxidative stress may function to compensate the impaired nitric oxide-dependent vasorelaxation in hypertension and atherosclerosis. (C) Lippincott Williams and Wilkins.

KW - Adrenomedullin

KW - Endothelial cells

KW - Hydrogen peroxide

KW - N-acetylcysteine

KW - Natriuretic peptide

KW - Oxidative stress

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M3 - Article

C2 - 10826560

AN - SCOPUS:0034033539

VL - 18

SP - 575

EP - 580

JO - Journal of Hypertension

JF - Journal of Hypertension

SN - 0263-6352

IS - 5

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