Oxidative stress suppresses the endothelial secretion of endothelin

T. Saito; H. Itoh; T. Chun; T. Igaki; Y. Mori; J. Yamashita; K. Doi; T. Tanaka; M. Inoue; K. Masatsugu; Y. Fukunaga; N. Sawada; K. Tojo; Y. Saito; T. Hosoya; K. Nakao

doi:10.1097/00005344-199800001-00096

Oxidative stress suppresses the endothelial secretion of endothelin

T. Saito, H. Itoh, T. Chun, T. Igaki, Y. Mori, J. Yamashita, K. Doi, T. Tanaka, M. Inoue, K. Masatsugu, Y. Fukunaga, N. Sawada, K. Tojo, Y. Saito, T. Hosoya, K. Nakao

Research output: Contribution to journal › Article › peer-review

8 Citations (Scopus)

Abstract

To address endothelial function on vascular walls exposed to oxidative stress, we investigated the effect of oxidative stress on the secretion of endothelin-1 (ET-1) from cultured bovine carotid artery endothelial cells (BAECs). Concentrations of ET-1 in the media were measured by a specific radioimmunoassay and ET-1 mRNA expression was estimated by Northern blot analysis. Treatment of BAECs with 0.5-2.0 mM H₂O₂ for 3 h suppressed both ET-1 secretion and ET-1 mRNA expression in a dose-dependent manner compared to control. Attenuation of ET-1 mRNA expression by H₂O₂ was revealed to take place at the transcriptional level. The addition of N^G-nitro-L-arginine-methyl ester (L-NAME) 10 μm, a specific nitric oxide synthase inhibitor, had no effect on H₂O₂-induced suppression of ET-1 mRNA expression. Suppression of ET secretion under oxidative stress observed in the present study is proposed to be a compensatory mechanism of endothelial cells to inhibit vasoconstriction and proliferation during oxidative stress.

Original language	English
Pages (from-to)	S345-S347
Journal	Journal of Cardiovascular Pharmacology
Volume	31
Issue number	SUPPL. 1
DOIs	https://doi.org/10.1097/00005344-199800001-00096
Publication status	Published - 1998
Externally published	Yes

Keywords

Endothelial cells
Endothelin
Hydrogen peroxide
L-NAME
Oxidative stress

ASJC Scopus subject areas

Pharmacology
Cardiology and Cardiovascular Medicine

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10.1097/00005344-199800001-00096

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Saito, T., Itoh, H., Chun, T., Igaki, T., Mori, Y., Yamashita, J., Doi, K., Tanaka, T., Inoue, M., Masatsugu, K., Fukunaga, Y., Sawada, N., Tojo, K., Saito, Y., Hosoya, T., & Nakao, K. (1998). Oxidative stress suppresses the endothelial secretion of endothelin. Journal of Cardiovascular Pharmacology, 31(SUPPL. 1), S345-S347. https://doi.org/10.1097/00005344-199800001-00096

Saito, T, Itoh, H, Chun, T, Igaki, T, Mori, Y, Yamashita, J, Doi, K, Tanaka, T, Inoue, M, Masatsugu, K, Fukunaga, Y, Sawada, N, Tojo, K, Saito, Y, Hosoya, T & Nakao, K 1998, 'Oxidative stress suppresses the endothelial secretion of endothelin', Journal of Cardiovascular Pharmacology, vol. 31, no. SUPPL. 1, pp. S345-S347. https://doi.org/10.1097/00005344-199800001-00096

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abstract = "To address endothelial function on vascular walls exposed to oxidative stress, we investigated the effect of oxidative stress on the secretion of endothelin-1 (ET-1) from cultured bovine carotid artery endothelial cells (BAECs). Concentrations of ET-1 in the media were measured by a specific radioimmunoassay and ET-1 mRNA expression was estimated by Northern blot analysis. Treatment of BAECs with 0.5-2.0 mM H2O2 for 3 h suppressed both ET-1 secretion and ET-1 mRNA expression in a dose-dependent manner compared to control. Attenuation of ET-1 mRNA expression by H2O2 was revealed to take place at the transcriptional level. The addition of NG-nitro-L-arginine-methyl ester (L-NAME) 10 μm, a specific nitric oxide synthase inhibitor, had no effect on H2O2-induced suppression of ET-1 mRNA expression. Suppression of ET secretion under oxidative stress observed in the present study is proposed to be a compensatory mechanism of endothelial cells to inhibit vasoconstriction and proliferation during oxidative stress.",

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author = "T. Saito and H. Itoh and T. Chun and T. Igaki and Y. Mori and J. Yamashita and K. Doi and T. Tanaka and M. Inoue and K. Masatsugu and Y. Fukunaga and N. Sawada and K. Tojo and Y. Saito and T. Hosoya and K. Nakao",

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T1 - Oxidative stress suppresses the endothelial secretion of endothelin

AU - Saito, T.

AU - Itoh, H.

AU - Chun, T.

AU - Igaki, T.

AU - Mori, Y.

AU - Yamashita, J.

AU - Doi, K.

AU - Tanaka, T.

AU - Inoue, M.

AU - Masatsugu, K.

AU - Fukunaga, Y.

AU - Sawada, N.

AU - Tojo, K.

AU - Saito, Y.

AU - Hosoya, T.

AU - Nakao, K.

PY - 1998

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N2 - To address endothelial function on vascular walls exposed to oxidative stress, we investigated the effect of oxidative stress on the secretion of endothelin-1 (ET-1) from cultured bovine carotid artery endothelial cells (BAECs). Concentrations of ET-1 in the media were measured by a specific radioimmunoassay and ET-1 mRNA expression was estimated by Northern blot analysis. Treatment of BAECs with 0.5-2.0 mM H2O2 for 3 h suppressed both ET-1 secretion and ET-1 mRNA expression in a dose-dependent manner compared to control. Attenuation of ET-1 mRNA expression by H2O2 was revealed to take place at the transcriptional level. The addition of NG-nitro-L-arginine-methyl ester (L-NAME) 10 μm, a specific nitric oxide synthase inhibitor, had no effect on H2O2-induced suppression of ET-1 mRNA expression. Suppression of ET secretion under oxidative stress observed in the present study is proposed to be a compensatory mechanism of endothelial cells to inhibit vasoconstriction and proliferation during oxidative stress.

AB - To address endothelial function on vascular walls exposed to oxidative stress, we investigated the effect of oxidative stress on the secretion of endothelin-1 (ET-1) from cultured bovine carotid artery endothelial cells (BAECs). Concentrations of ET-1 in the media were measured by a specific radioimmunoassay and ET-1 mRNA expression was estimated by Northern blot analysis. Treatment of BAECs with 0.5-2.0 mM H2O2 for 3 h suppressed both ET-1 secretion and ET-1 mRNA expression in a dose-dependent manner compared to control. Attenuation of ET-1 mRNA expression by H2O2 was revealed to take place at the transcriptional level. The addition of NG-nitro-L-arginine-methyl ester (L-NAME) 10 μm, a specific nitric oxide synthase inhibitor, had no effect on H2O2-induced suppression of ET-1 mRNA expression. Suppression of ET secretion under oxidative stress observed in the present study is proposed to be a compensatory mechanism of endothelial cells to inhibit vasoconstriction and proliferation during oxidative stress.

KW - Endothelial cells

KW - Endothelin

KW - Hydrogen peroxide

KW - L-NAME

KW - Oxidative stress

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Oxidative stress suppresses the endothelial secretion of endothelin

Abstract

Keywords

ASJC Scopus subject areas

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