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1 Department of Emergency Medicine, University of Pennsylvania Medical Center, Philadelphia, PA, USA; Institute for Environmental Medicine, University of Pennsylvania Medical Center, Philadelphia, PA, USA
2 Institute for Environmental Medicine, University of Pennsylvania Medical Center, Philadelphia, PA, USA
3 Philadelphia Biomedical Research Institute, King of Prussia, PA, USA
4 Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
5 Department of Biochemistry and Biophysics, University of Pennsylvania Medical Center, Philadelphia, PA, USA
6 Department of Physiology, University of Pennsylvania Medical Center, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: sthom{at}mail.med.upenn.edu.
We hypothesized that elevated partial pressures of O2 would increase perivascular nitric oxide (.NO) synthesis. Rodents with O2- and .NO -specific microelectrodes implanted adjacent to the abdominal aorta were exposed to O2 at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA). Exposures to 2.0 and 2.8 ATA O2 stimulated type I nitric oxide 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 O2 appeared to be due to altered cellular redox state. Exposure to 2.8 ATA O2, but not 2.0 ATA O2, 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 (HSP90). Infusion of superoxide dismutase inhibited .NO elevation at 2.8, but not 2.0 ATA O2. 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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