Oxygen Dependency of Hydrogen Sulfide‐mediated Vasoconstriction in Cyclostome Aortas

Hydrogen sulfide (H 2 S) is a vasoregulatory molecule and recent evidence suggests it may be an O 2 sensor for hypoxic vasoconstriction (HVC). Here we examined H 2 S ‐ O 2 interactions in hagfish vessels. In myographic studies, H 2 S (Na 2 S) dose‐dependently constricted dorsal aortas (DA) and efferent branchial arteries (EBA) but did affect ventral aorta or afferent branchial arteries; hypoxia produces similar responses. Hypoxia enhanced DA sensitivity to H 2 S. HVC in DA was augmented by the H 2 S precursor cysteine and inhibited by aminooxy acetate (AOA), an inhibitor of the H 2 S‐synthesizing enzyme, CBS. HVC was unaffected by propargyl glycine, the CSE inhibitor. DA O 2 consumption (MO 2 ) was constant between PO 2 15–115 mmHg, but decreased when PO 2 <15 mmHg and increased after PO 2 exceeded 115 mmHg. 10 uM H 2 S increased MO 2 , whereas MO 2 fell when [H 2 S] >100 uM. Consistent with the effects on HVC, cysteine increased and AOA decreased MO 2 . These results show that H 2 S is a monophasic vasoconstrictor of specific cyclostome vessels and because hagfish lack vascular NO, and vascular sensitivity was enhanced at low PO 2 , it is unlikely that H 2 S contractions are mediated by either H 2 S‐NO interaction or an oxidation product of H 2 S. They also support the hypothesis that H 2 S metabolism is an O 2 sensor in vertebrate vascular smooth muscle. Support: NSF IBN 0235223, IOS 0641436 and Erskin Fellowship (KRO)