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

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Pages (from-to)575-580
Number of pages6
JournalJournal of hypertension
Volume18
Issue number5
DOIs
Publication statusPublished - Jan 1 2000

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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

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

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.

In: Journal of hypertension, Vol. 18, No. 5, 01.01.2000, p. 575-580.

Research output: Contribution to journalArticle

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, vol. 18, no. 5, pp. 575-580. https://doi.org/10.1097/00004872-200018050-00010
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. In: Journal of hypertension. 2000 ; Vol. 18, No. 5. pp. 575-580.
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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.",
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",
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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 - 2000/1/1

Y1 - 2000/1/1

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.

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