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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 (P
0.05).
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