期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 109, 期 4, 页码 1293-1298出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1119658109
关键词
gas biology; neurovascular unit; energy metabolism; gasotransmitter
资金
- Japan Science and Technology Agency
- Exploratory Research for Advanced Technology
- Suematsu Gas Biology Project
- Japan Society for the Promotion of Science [21500353]
- US Public Health Service [MH018501]
- Ministry of Economy, Technology and Industry of Japan
- Ministry of Education, Culture, Sports, Science, and Technology Japan
- National Institutes of Health [T32 GM007309]
- Grants-in-Aid for Scientific Research [21500353] Funding Source: KAKEN
Enhancement of cerebral blood flow by hypoxia is critical for brain function, but signaling systems underlying its regulation have been unclear. We report a pathway mediating hypoxia-induced cerebral vasodilation in studies monitoring vascular disposition in cerebellar slices and in intact mouse brains using two-photon intravital laser scanning microscopy. In this cascade, hypoxia elicits cerebral vasodilation via the coordinate actions of H2S formed by cystathionine beta-synthase (CBS) and CO generated by heme oxygenase (HO)-2. Hypoxia diminishes CO generation by HO-2, an oxygen sensor. The constitutive CO physiologically inhibits CBS, and hypoxia leads to increased levels of H2S that mediate the vasodilation of precapillary arterioles. Mice with targeted deletion of HO-2 or CBS display impaired vascular responses to hypoxia. Thus, in intact adult brain cerebral cortex of HO-2-null mice, imaging mass spectrometry reveals an impaired ability to maintain ATP levels on hypoxia.
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