Fig. 6. Contribution of the H₂S precursor, cysteine, to hypoxic responses. (A) Addition of cysteine to lamprey dorsal aorta (DA) significantly and specifically increases the magnitude of a hypoxic contraction. In the absence of exogenous cysteine, a hypoxic contraction (N₂) develops as much force as a reference 80 mmol l^–1 KCl contraction (broken line). Addition of cysteine (Cys; 1 mmol l^–1) produces a slight, transient contraction, doubles the strength of the hypoxic contraction (N₂+Cys; P0.05), but does not affect a second KCl contraction. Addition of glycine (Gly; 1 mmol l^–1) also produced a slight contraction but did not affect either hypoxic (N₂+GLY) or KCl (KCl+Gly) contractions. (B) Rat thoracic aortas (TA) were exposed to hypoxia for 15 h in the absence (Con) or presence of cysteine (Cys), returned to normoxia, pre-contracted with U-46619, and exposed twice to hypoxia. Incubation with cysteine significantly (P0.05) reduced the magnitude of the first hypoxic relaxation but enabled the vessels to respond to re-oxygenation and a second hypoxia. (C) Bovine pulmonary arteries (PA) were exposed to hypoxia for 15 h in the absence (Con) or presence of cysteine (Cys), returned to normoxia, pre-contracted with U-46619, and exposed twice to hypoxia. Incubation with cysteine increased the magnitude of the initial hypoxic contraction and the second hypoxic contraction was sustained longer.