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Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability

Gomisin A (GA) is a small molecular weight lignan present in Schisandra chinensis, and has been demonstrated to have vasodilatory activity. In the present study, we investigated the effect of GA on blood pressure (BP) in angiotensin II (Ang II)-induced hypertensive mice. C57/BL6 mice infused subcuta...

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Autores principales: Young Park, Ji, Wook Yun, Jung, Whan Choi, Young, Ung Bae, Jin, Won Seo, Kyo, Jin Lee, Seung, Youn Park, So, Whan Hong, Ki, Kim, Chi Dae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434368/
https://www.ncbi.nlm.nih.gov/pubmed/22534517
http://dx.doi.org/10.1038/hr.2012.50
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author Young Park, Ji
Wook Yun, Jung
Whan Choi, Young
Ung Bae, Jin
Won Seo, Kyo
Jin Lee, Seung
Youn Park, So
Whan Hong, Ki
Kim, Chi Dae
author_facet Young Park, Ji
Wook Yun, Jung
Whan Choi, Young
Ung Bae, Jin
Won Seo, Kyo
Jin Lee, Seung
Youn Park, So
Whan Hong, Ki
Kim, Chi Dae
author_sort Young Park, Ji
collection PubMed
description Gomisin A (GA) is a small molecular weight lignan present in Schisandra chinensis, and has been demonstrated to have vasodilatory activity. In the present study, we investigated the effect of GA on blood pressure (BP) in angiotensin II (Ang II)-induced hypertensive mice. C57/BL6 mice infused subcutaneously with Ang II (1 and 2 μg kg(−1) per min for 2 weeks) showed an increase in BP with a decrease in nitric oxide (NO) metabolites in plasma, and a negative correlation between these two parameters was demonstrated. In the thoracic aorta from Ang II-induced hypertensive mice, a decrease in vascular NO that was accompanied by a diminution of phosphorylated endothelial nitric oxide synthase (eNOS), as well as by increased reactive oxygen species (ROS) production, was demonstrated. These alterations in BP, eNOS phosphorylation and ROS production in the vasculature of Ang II-treated mice were markedly and dose-dependently reversed by simultaneous administration of GA (2 and 10 μg kg(−1) per min). In addition, Ang II-induced ROS production in cultured vascular cells such as endothelial cells and vascular smooth muscle cells was markedly attenuated by GA. These results suggested that GA attenuated the increase in BP via preservation of vascular NO bioavailability not only by inhibiting ROS production but also by preventing the impairment of eNOS function in the vasculature of Ang II-induced hypertensive mice.
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spelling pubmed-34343682012-09-06 Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability Young Park, Ji Wook Yun, Jung Whan Choi, Young Ung Bae, Jin Won Seo, Kyo Jin Lee, Seung Youn Park, So Whan Hong, Ki Kim, Chi Dae Hypertens Res Original Article Gomisin A (GA) is a small molecular weight lignan present in Schisandra chinensis, and has been demonstrated to have vasodilatory activity. In the present study, we investigated the effect of GA on blood pressure (BP) in angiotensin II (Ang II)-induced hypertensive mice. C57/BL6 mice infused subcutaneously with Ang II (1 and 2 μg kg(−1) per min for 2 weeks) showed an increase in BP with a decrease in nitric oxide (NO) metabolites in plasma, and a negative correlation between these two parameters was demonstrated. In the thoracic aorta from Ang II-induced hypertensive mice, a decrease in vascular NO that was accompanied by a diminution of phosphorylated endothelial nitric oxide synthase (eNOS), as well as by increased reactive oxygen species (ROS) production, was demonstrated. These alterations in BP, eNOS phosphorylation and ROS production in the vasculature of Ang II-treated mice were markedly and dose-dependently reversed by simultaneous administration of GA (2 and 10 μg kg(−1) per min). In addition, Ang II-induced ROS production in cultured vascular cells such as endothelial cells and vascular smooth muscle cells was markedly attenuated by GA. These results suggested that GA attenuated the increase in BP via preservation of vascular NO bioavailability not only by inhibiting ROS production but also by preventing the impairment of eNOS function in the vasculature of Ang II-induced hypertensive mice. Nature Publishing Group 2012-09 2012-04-26 /pmc/articles/PMC3434368/ /pubmed/22534517 http://dx.doi.org/10.1038/hr.2012.50 Text en Copyright © 2012 The Japanese Society of Hypertension http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Original Article
Young Park, Ji
Wook Yun, Jung
Whan Choi, Young
Ung Bae, Jin
Won Seo, Kyo
Jin Lee, Seung
Youn Park, So
Whan Hong, Ki
Kim, Chi Dae
Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability
title Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability
title_full Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability
title_fullStr Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability
title_full_unstemmed Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability
title_short Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability
title_sort antihypertensive effect of gomisin a from schisandra chinensis on angiotensin ii-induced hypertension via preservation of nitric oxide bioavailability
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434368/
https://www.ncbi.nlm.nih.gov/pubmed/22534517
http://dx.doi.org/10.1038/hr.2012.50
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