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1 Biology, University of Alabama at Birmingham, Birmingham, Alabama, United States
2 Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States
3 Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, Alabama, United States
4 Anesthesiology, University of Alabama, Birmingham, Alabama, United States
5 Environmental Health Sciences, University of Alabama, Birmingham, Birmingham, Alabama, United States
* To whom correspondence should be addressed. E-mail: dwkraus{at}uab.edu.
Hydrogen sulfide (H2S) has recently been shown to have a signaling role in vascular cells. Like nitric oxide (NO), H2S is enzymatically produced by amino acid metabolism and can cause post-translational modification of proteins, particularly at thiol residues. Molecular targets for H2S include KATP channels, and H2S may interact with NO and heme proteins such as cyclooxygenase. It is well known that the reactions of NO in the vasculature are O2-dependent but this has not been addressed in most studies designed to elucidate the role of H2S in vascular function. This is important since H2S reactions can be dramatically altered by the high concentrations of O2 used in cell culture and organ bath experiments. In order to test the hypothesis that the effects of H2S on the vasculature are O2-dependent, we have measured real time levels of H2S and O2 in respirometry and vessel tension experiments as well as the associated vascular responses. A novel polarographic hydrogen sulfide sensor (PHSS) developed in our laboratory was used to measure H2S levels. Here we report that in rat aorta, H2S concentrations that mediate rapid contraction at high O2 levels cause rapid relaxation at lower physiological O2 levels. At high O2, the vasoconstrictive effect of H2S suggests that it may not be H2S per se but a putative vasoactive oxidation product that mediates constriction. These data are interpreted in terms of the potential for H2S to modulate vascular tone in vivo.
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