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Fig. 4. Effects of (A) L-cysteine, the substrate for H₂S synthesis, (B) the cystathionine β-synthase inhibitor, amino-oxyacetate (AOA), (C) the cystathionine -lyase inhibitor, propargyl glycine (PPG) and (D) an uncoupler of pyridoxyl 5'-phosphate-dependent enzymes, hydroxylamine (HA) on hypoxic (100% N₂) vasoconstriction of hagfish dorsal aorta. Vessels were continuously contracted with N₂ then given cumulative additions of cysteine or inhibitors followed by 10 µmol l^–1 carbachol (CBC). Values are expressed as the average tension (mean ± s.e.m.) as the percentage of the reference carbachol contraction (100%; dashed line). Hypoxic contractions (N₂) were generally 30% of the reference carbachol contraction. Cysteine at 1 mmol l^–1 approximately doubled the force of the original N₂ contraction, whereas raising cysteine to 10 mmol l^–1 relaxed the vessels back to the original N₂ level (^* significant increase from N₂; significant decrease from 1 mmol l^–1 cysteine; N=7). Hypoxic contractions were unaffected by 100 µmol l^–1 and 1 mmol l^–1 AOA. At 4 mmol l^–1 AOA, the hypoxic contraction was completely inhibited (^*; N=8). PPG did not significantly affect the N₂ contraction (N=8). HA, 10 µmol l^–1 HA significantly (^*) increased the force of the N₂ contraction and tension was maintained at 100 µmol l^–1 and 1 mmol l^–1 (N=8).

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