期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 284, 期 4, 页码 H1230-H1239出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.01043.2002
关键词
neuronal nitric oxide synthase; heat shock protein 90; calmodulin; hyperbaric oxygen
资金
- NCCIH NIH HHS [AT-00428] Funding Source: Medline
- NCI NIH HHS [CA-82506] Funding Source: Medline
- NIEHS NIH HHS [ES-05211] Funding Source: Medline
- NIGMS NIH HHS [GM-30736] Funding Source: Medline
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.
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