Journal
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
Volume 70, Issue 11, Pages 1355-1359Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glu244
Keywords
Hypertension; Middle cerebral artery; Oxidative stress; Mitochondrion; Free radicals
Categories
Funding
- American Heart Association
- Oklahoma Center for the Advancement of Science and Technology
- Hungarian National Science Research Fund (OTKA) [K 108444]
- grant: Developing Competitiveness of Universities in the South Transdanubian Region, Identification of new bio-markers ..., [SROP-4.2.2.A-11/1/KONV-2012-0017]
- grant: Complex examination of neuropeptides ... , [SROP-4.2.2. A-11/1/KONV-2012-0024]
- National Center for Complementary and Alternative Medicine [R01-AT006526]
- National Institute on Aging [R01-AG031085, R01-AG038747, R01-NS056218]
- Ellison Medical Foundation
- Arkansas Claude Pepper Older Americans Independence Center at University of Arkansas Medical Center [P30 AG028718]
- European Union
- State of Hungary
- European Social Fund, National Excellence Program [TAMOP 4.2.4.A/2-11-1-2012-0001]
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Epidemiological studies demonstrate that in addition to the increased prevalence of hypertension in old patients, the deleterious cerebrovascular effects of hypertension ( including atherosclerosis, stroke, and vascular cognitive impairment) are also exacerbated in elderly individuals. The cellular mechanisms by which aging and hypertension interact to promote cerebrovascular pathologies are not well understood. To test the hypothesis that aging exacerbates high pressure-induced mitochondrial oxidative stress, we exposed isolated segments of the middle cerebral arteries of young ( 3 months) and aged ( 24 months) C57BL/6 mice to 60 or 140 mmHg intraluminal pressure and assessed changes in mitochondrial reactive oxygen species production using a mitochondria-targeted redox-sensitive fluorescent indicator dye ( MitoSox) by confocal microscopy. Perinuclear MitoSox fluorescence was significantly stronger in high pressure-exposed middle cerebral arteries compared with middle cerebral arteries of the same animals exposed to 60 mmHg, indicating that high pressure increases mitochondrial reactive oxygen species production in the smooth muscle cells of cerebral arteries. Comparison of young and aged middle cerebral arteries showed that aging exacerbates high pressure-induced mitochondrial reactive oxygen species production in cerebral arteries. We propose that increased mechanosensitive mitochondrial oxidative stress may potentially exacerbate cerebrovascular injury and vascular inflammation in aging.
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