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First published online June 27, 2008
Journal of Experimental Biology 211, 2205-2213 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.016766

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Oxygen dependency of hydrogen sulfide-mediated vasoconstriction in cyclostome aortas

Kenneth R. Olson^1,*, Leonard G. Forgan², Ryan A. Dombkowski³ and Malcolm E. Forster²

¹ Indiana University School of Medicine–South Bend, 1234 Notre Dame Avenue, South Bend, IN 46617, USA
² School of Biological Sciences, University of Canterbury, Private Bag 4800, Christchurch 8020, New Zealand
³ Department of Biology, Saint Mary's College, Notre Dame, IN 46556, USA

^* Author for correspondence (e-mail: kolson{at}nd.edu)

Accepted 10 April 2008

Hydrogen sulfide (H₂S) has been proposed to mediate hypoxic vasoconstriction (HVC), however, other studies suggest the vasoconstrictory effect indirectly results from an oxidation product of H₂S. Here we examined the relationship between H₂S and O₂ in isolated hagfish and lamprey vessels that exhibit profound hypoxic vasoconstriction. In myographic studies, H₂S (Na₂S) dose-dependently constricted dorsal aortas (DA) and efferent branchial arteries (EBA) but did not affect ventral aortas or afferent branchial arteries; effects similar to those produced by hypoxia. Sensitivity of H₂S-mediated contraction in hagfish and lamprey DA was enhanced by hypoxia. HVC in hagfish DA was enhanced by the H₂S precursor cysteine and inhibited by amino-oxyacetate, an inhibitor of the H₂S-synthesizing enzyme, cystathionine β-synthase. HVC was unaffected by propargyl glycine, an inhibitor of cystathionine -lyase. Oxygen consumption (_O2) of hagfish DA was constant between 15 and 115 mmHg P_O2 (1 mmHg=0.133 kPa), decreased when P_O2 <15 mmHg, and increased after P_O2 exceeded 115 mmHg. 10 µmol l^–1 H₂S increased and 100 µmol l^–1 H₂S decreased _O2. Consistent with the effects on HVC, cysteine increased and amino-oxyacetate decreased _O2. These results show that H₂S is a monophasic vasoconstrictor of specific cyclostome vessels and because hagfish lack vascular NO, and vascular sensitivity to H₂S was enhanced at low P_O2, it is unlikely that H₂S contractions are mediated by either H₂S–NO interaction or an oxidation product of H₂S. These experiments also provide additional support for the hypothesis that the metabolism of H₂S is involved in oxygen sensing/signal transduction in vertebrate vascular smooth muscle.

Key words: hypoxic vasoconstriction, oxygen sensing, vascular smooth muscle

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