Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension
Joint Authors
Oelze, Matthias
Daiber, Andreas
Münzel, Thomas
Steven, Sebastian
Brandt, Moritz
Ullmann, Elisabeth
Kröller-Schön, Swenja
Heeren, Tjebo
Tran, Lan P.
Daub, Steffen
Dib, Mobin
Stalleicken, Dirk
Wenzel, Philip
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-02-28
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Objective.
Oxidative stress and endothelial dysfunction contribute to pulmonary arterial hypertension (PAH).
The role of the nitrovasodilator pentaerythritol tetranitrate (PETN) on endothelial function and oxidative stress in PAH has not yet been defined.
Methods and Results.
PAH was induced by monocrotaline (MCT, i.v.) in Wistar rats.
Low (30 mg/kg; MCT30), middle (40 mg/kg; MCT40), or high (60 mg/kg; MCT60) dose of MCT for 14, 28, and 42 d was used.
MCT induced endothelial dysfunction, pulmonary vascular wall thickening, and fibrosis, as well as protein tyrosine nitration.
Pulmonary arterial pressure and heart/body and lung/body weight ratio were increased in MCT40 rats (28 d) and reduced by oral PETN (10 mg/kg, 24 d) therapy.
Oxidative stress in the vascular wall, in the heart, and in whole blood as well as vascular endothelin-1 signaling was increased in MCT40-treated rats and normalized by PETN therapy, likely by upregulation of heme oxygenase-1 (HO-1).
PETN therapy improved endothelium-dependent relaxation in pulmonary arteries and inhibited endothelin-1-induced oxidative burst in whole blood and the expression of adhesion molecule (ICAM-1) in endothelial cells.
Conclusion.
MCT-induced PAH impairs endothelial function (aorta and pulmonary arteries) and increases oxidative stress whereas PETN markedly attenuates these adverse effects.
Thus, PETN therapy improves pulmonary hypertension beyond its known cardiac preload reducing ability.
American Psychological Association (APA)
Steven, Sebastian& Oelze, Matthias& Brandt, Moritz& Ullmann, Elisabeth& Kröller-Schön, Swenja& Heeren, Tjebo…[et al.]. 2017. Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-13.
https://search.emarefa.net/detail/BIM-1194696
Modern Language Association (MLA)
Steven, Sebastian…[et al.]. Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-13.
https://search.emarefa.net/detail/BIM-1194696
American Medical Association (AMA)
Steven, Sebastian& Oelze, Matthias& Brandt, Moritz& Ullmann, Elisabeth& Kröller-Schön, Swenja& Heeren, Tjebo…[et al.]. Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-13.
https://search.emarefa.net/detail/BIM-1194696
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1194696