TY - JOUR
T1 - Site of action of endogenous nitric oxide on pulmonary vasculature in rats
AU - Ferrario, Lara
AU - Amin, Hesham M.
AU - Sugimori, Kunio
AU - Camporesi, Enrico M.
AU - Hakim, Tawfic S.
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1996
Y1 - 1996
N2 - The effect of endogenous nitric oxide (NO) on the pulmonary hypoxic vasoconstriction was studied in isolated and blood perfused rat lungs. By applying the occlusion technique we partitioned the total pulmonary vascular resistance (PVR) into four segments: (1) large arteries (R(a)), (2) small arteries (R(a')), (3) small veins (R(v')), and (4) large veins (R(v)). The resistances were evaluated under baseline (BL) conditions and during; hypoxic vasoconstriction and acetylcholine (Ach) which was injected during hypoxic vasoconstriction. After recovery from hypoxia and Ach, N(ω)-nitro-L-arginine (L-NA) was added to the reservoir and the responses to hypoxia and Ach were reevaluated. Before L-NA, hypoxia caused significant increase in the resistances of all segments (P < 0.05), with the largest being in R(a) and R(a'). Ach-induced relaxation during hypoxia occurred in R(a), R(a') and R(v') (P < 0.05). L-NA did not change the basal tone of the pulmonary vasculature significantly. However, after L-NA, hypoxic vasoconstriction was markedly enhanced in R(a), R(a'), and R(v') (P < 0.01) compared with the hypoxic response before L-NA. Ach-induced relaxation was abolished after L-NA. We conclude that, in rat lungs, inhibition of NO production during hypoxia enhances the response in the small arteries and veins as well as in the large arteries. The results suggest that hypoxic vasoconstriction in the large pulmonary arteries and small vessels is attenuated by NO release.
AB - The effect of endogenous nitric oxide (NO) on the pulmonary hypoxic vasoconstriction was studied in isolated and blood perfused rat lungs. By applying the occlusion technique we partitioned the total pulmonary vascular resistance (PVR) into four segments: (1) large arteries (R(a)), (2) small arteries (R(a')), (3) small veins (R(v')), and (4) large veins (R(v)). The resistances were evaluated under baseline (BL) conditions and during; hypoxic vasoconstriction and acetylcholine (Ach) which was injected during hypoxic vasoconstriction. After recovery from hypoxia and Ach, N(ω)-nitro-L-arginine (L-NA) was added to the reservoir and the responses to hypoxia and Ach were reevaluated. Before L-NA, hypoxia caused significant increase in the resistances of all segments (P < 0.05), with the largest being in R(a) and R(a'). Ach-induced relaxation during hypoxia occurred in R(a), R(a') and R(v') (P < 0.05). L-NA did not change the basal tone of the pulmonary vasculature significantly. However, after L-NA, hypoxic vasoconstriction was markedly enhanced in R(a), R(a'), and R(v') (P < 0.01) compared with the hypoxic response before L-NA. Ach-induced relaxation was abolished after L-NA. We conclude that, in rat lungs, inhibition of NO production during hypoxia enhances the response in the small arteries and veins as well as in the large arteries. The results suggest that hypoxic vasoconstriction in the large pulmonary arteries and small vessels is attenuated by NO release.
KW - Acetylcholine
KW - Double occlusion technique
KW - Hypoxia
KW - Nitric oxide
KW - Pulmonary vasculature
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U2 - 10.1007/s004240050165
DO - 10.1007/s004240050165
M3 - Article
C2 - 8766013
AN - SCOPUS:0030057169
SN - 0031-6768
VL - 432
SP - 523
EP - 527
JO - Pflugers Archiv European Journal of Physiology
JF - Pflugers Archiv European Journal of Physiology
IS - 3
ER -