Journal article
Stimulation of perivascular nitric oxide synthesis by oxygen
American journal of physiology. Heart and circulatory physiology, v 284(4), pp H1230-H1239
01 Apr 2003
PMID: 12505879
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
We hypothesized that elevated partial pressures of O
2
would increase perivascular nitric oxide (·NO) synthesis. Rodents with O
2
- and ·NO-specific microelectrodes implanted adjacent to the abdominal aorta were exposed to O
2
at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA). Exposures to 2.0 and 2.8 ATA O
2
stimulated neuronal (type I) NO synthase (nNOS) and significantly increased steady-state ·NO concentration, but the mechanism for enzyme activation differed at each partial pressure. At both pressures, elevations in ·NO concentration were inhibited by the nNOS inhibitor 7-nitroindazole and the calcium channel blocker nimodipine. Enzyme activation at 2.0 ATA O
2
appeared to be due to an altered cellular redox state. Exposure to 2.8 ATA O
2
, but not 2.0 ATA O
2
, increased nNOS activity by enhancing nNOS association with calmodulin, and an inhibitory effect of geldanamycin indicated that the association was facilitated by heat shock protein 90. Infusion of superoxide dismutase inhibited ·NO elevation at 2.8 but not 2.0 ATA O
2
. Hyperoxia increased the concentration of ·NO associated with hemoglobin. These findings highlight the complexity of oxidative stress responses and may help explain some of the dose responses associated with therapeutic applications of hyperbaric oxygen.
Metrics
Details
- Title
- Stimulation of perivascular nitric oxide synthesis by oxygen
- Creators
- Stephen R. Thom - Department of Emergency Medicine andDonald Fisher - Institute for Environmental ManagementJie Zhang - Institute for Environmental ManagementVeena M. Bhopale - Institute for Environmental ManagementS. Tsuyoshi Ohnishi - Philadelphia Biomedical Research Institute, King of Prussia, Pennsylvania 19406; andYashige Kotake - Oklahoma Medical Research FoundationTomoko Ohnishi - Biophysics andDonald G. Buerk - University of Pennsylvania
- Publication Details
- American journal of physiology. Heart and circulatory physiology, v 284(4), pp H1230-H1239
- Publisher
- American Physiological Society (APS)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems
- Web of Science ID
- WOS:000181425900024
- Scopus ID
- 2-s2.0-0037379061
- Other Identifier
- 991019231752204721
UN Sustainable Development Goals (SDGs)
This publication has contributed to the advancement of the following goals:
InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Cardiac & Cardiovascular Systems
- Peripheral Vascular Disease
- Physiology