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Oxidative Stress and Endothelial Dysfunction in Pulmonary Arteries of Aged Rats
Author(s) -
Ungvari Zoltan,
Ballabh Praveen,
Podlutsky Andrej,
Csiszar Anna
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.775.4
Subject(s) - oxidative stress , endothelial dysfunction , medicine , pulmonary artery , pulmonary hypertension , enos , endocrinology , endothelium , cardiology , glutathione peroxidase , catalase , nitric oxide , nitric oxide synthase
Aging in the systemic circulation is associated with generalized endothelial dysfunction and increased oxidative stress, which are thought to contribute to the increased morbidity and mortality of cardiovascular diseases in the elderly. Previous studies have shown that pulmonary artery pressure and vascular resistance increase with normal aging in humans, yet age‐related functional and phenotypic changes in the pulmonary arteries have not been characterized. To determine whether in the pulmonary circulation aging elicits endothelial dysfunction and oxidative stress, isolated pulmonary arteries of young (3 m.o.) and aged (28 m.o.) F344 rats were compared. We found that aging in rat pulmonary arteries is associated with impaired acetylcholine‐induced relaxation and vascular oxidative stress. Endothelial dysfunction in the aged pulmonary vessels is reversed by inhibition of NAD(P)H oxidase. Expression of gp91phox, Nox‐1 and Nox‐4 tends to increase in aged vessels. In pulmonary arteries of aged rats expression of eNOS, Cu,Zn‐SOD, Mn‐SOD and glutathione peroxidase is unaltered, whereas expression of catalase is significantly decreased. Our results suggest that aging is associated with oxidative stress and endothelial dysfunction in the pulmonary arteries, which may contribute to the age‐related functional alterations in the pulmonary circulation.