Hydrogen sulfide mediates vasoactivity in an O2-dependent manner

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 292; no. 4; pp. H1953 - H1960
• Main Authors: Koenitzer, Jeffrey R, Isbell, T. Scott, Patel, Hetal D, Benavides, Gloria A, Dickinson, Dale A, Patel, Rakesh P, Darley-Usmar, Victor M, Lancaster, Jack R., Jr, Doeller, Jeannette E, Kraus, David W
• Format: Journal Article
• Language: English
• Published: United States 01.04.2007
• Subjects: Animals; Aorta - drug effects; Aorta - metabolism; Electron Transport - drug effects; Electron Transport - physiology; Female; Hydrogen Sulfide - metabolism; Hydrogen Sulfide - pharmacology; Male; Mitochondria - drug effects; Mitochondria - metabolism; Oxygen - metabolism; Oxygen Consumption - drug effects; Oxygen Consumption - physiology; Rats; Rats, Sprague-Dawley; Signal Transduction - drug effects; Signal Transduction - physiology; Vasodilation - drug effects; Vasodilation - physiology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.01193.2006

Departments of 1 Biology, 2 Pathology, 3 Environmental Health Sciences, and 4 Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama Submitted 31 October 2006 ; accepted in final form 7 December 2007 Hydrogen sulfide (H 2 S) has recently been shown to have a signaling role in vascular cells. Similar to nitric oxide (NO), H 2 S is enzymatically produced by amino acid metabolism and can cause posttranslational modification of proteins, particularly at thiol residues. Molecular targets for H 2 S include ATP-sensitive K + channels, and H 2 S may interact with NO and heme proteins such as cyclooxygenase. It is well known that the reactions of NO in the vasculature are O 2 dependent, but this has not been addressed in most studies designed to elucidate the role of H 2 S in vascular function. This is important, since H 2 S reactions can be dramatically altered by the high concentrations of O 2 used in cell culture and organ bath experiments. To test the hypothesis that the effects of H 2 S on the vasculature are O 2 dependent, we have measured real-time levels of H 2 S and O 2 in respirometry and vessel tension experiments, as well as the associated vascular responses. A novel polarographic H 2 S sensor developed in our laboratory was used to measure H 2 S levels. Here we report that, in rat aorta, H 2 S concentrations that mediate rapid contraction at high O 2 levels cause rapid relaxation at lower physiological O 2 levels. At high O 2 , the vasoconstrictive effect of H 2 S suggests that it may not be H 2 S per se but, rather, a putative vasoactive oxidation product that mediates constriction. These data are interpreted in terms of the potential for H 2 S to modulate vascular tone in vivo. aorta; sulfide sensor; oxygen consumption; vasorelaxation; mitochondria Address for reprint requests and other correspondence: D. W. Krauss, Dept. of Environmental Health Sciences, Univ. of Alabama at Birmingham, 1665 Univ. Blvd., Birmingham, AL 35294-0022 (e-mail: dwkraus{at}uab.edu )