Fig. 5. Constrictory and dilatory responses of isolated vessels to hypoxia (stippled bars) is partially or completely prevented by inhibition of H₂S synthesis (black bars). (A) Hypoxic vasoconstriction in lamprey dorsal aorta (DA; N=8) is unaffected by three consecutive bouts of N₂ exposure (left bars), whereas 1 mmol l^–1 of the pyridoxyl 5'-phosphate-dependent enzyme inhibitor, hydroxylamine (HA), reduces the N₂ response by over 80%. (B) Hypoxic vasodilation of norepinephrine (NE; 10^–5 mol l^–1) pre-contracted rat thoracic aorta (TA) is nearly completely blocked by PPG (N=6). (C) In NE pre-contracted rat pulmonary arteries (PA), both the hypoxic phase 1 contraction (1) and phase 2 relaxation (2) are partially inhibited by the CSE inhibitor, ß-cyanoalanine (BCA; 5 mmol l^–1) or a combination of 1 mmol l^–1 AOA, 10 mmol l^–1 BCA and 10 mmol l^–1 PPG (N=8 each group). (D) Hypoxic vasoconstriction in 10^–7 µmol l^–1 U-46619 pre-contracted (contraction not shown) bovine pulmonary arteries is unaffected by the CSE inhibitor D,L-propargylglycine (PPG; 10 mmol l^–1), partly blocked by the CBS inhibitor amino-oxyacetate (AOA; 1 mmol l^–1) and converted to slight relaxation by HA and a strong relaxation by a combination of the three inhibitors (N=6 each group). Values are means ± s.e.m.; *significantly different from respective control (P0.05).