TY - JOUR
T1 - Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo
AU - Persson, M. G.
AU - Gustafsson, L. E.
AU - Wiklund, N. P.
AU - Moncada, S.
AU - Hedqvist, P.
PY - 1990
Y1 - 1990
N2 - The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (F(IO2) = 21%) was 78 ± 16 cmH2O ml-1 min 1000-1 (mRU(L)). Hypoxic ventilation (F(IO2) = 10%) increased pulmonary vascular resistance to 117 ± 17 mRU(L). N(ω)-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 ± 28 mRU(L) and during hypoxic ventilation to 462 ± 80 mRU(L). During N(ω)-nitro-L-arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L-arginine reversed the effect of N(ω)-nitro-L-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 ± 26 mRU(L) and at hypoxic ventilation to 239 ± 42 mRU(L). In spontaneously breathing closed-chest rabbits, N(ω)-nitro-L-arginine methylester evoked a marked decrease in arterial P(O2) and increases in respiration frequency and central venous pressure, while blood pH, P(CO2) and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.
AB - The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (F(IO2) = 21%) was 78 ± 16 cmH2O ml-1 min 1000-1 (mRU(L)). Hypoxic ventilation (F(IO2) = 10%) increased pulmonary vascular resistance to 117 ± 17 mRU(L). N(ω)-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 ± 28 mRU(L) and during hypoxic ventilation to 462 ± 80 mRU(L). During N(ω)-nitro-L-arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L-arginine reversed the effect of N(ω)-nitro-L-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 ± 26 mRU(L) and at hypoxic ventilation to 239 ± 42 mRU(L). In spontaneously breathing closed-chest rabbits, N(ω)-nitro-L-arginine methylester evoked a marked decrease in arterial P(O2) and increases in respiration frequency and central venous pressure, while blood pH, P(CO2) and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.
KW - EDRF
KW - arginine analogues
KW - endothelium-derived relaxing factor
KW - hypoxia
KW - hypoxic pressor response
KW - nitric oxide
KW - pulmonary circulation
KW - vasoconstriction
UR - http://www.scopus.com/inward/record.url?scp=0025688846&partnerID=8YFLogxK
U2 - 10.1111/j.1748-1716.1990.tb09021.x
DO - 10.1111/j.1748-1716.1990.tb09021.x
M3 - Article
C2 - 1707210
AN - SCOPUS:0025688846
SN - 0001-6772
VL - 140
SP - 449
EP - 457
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
IS - 4
ER -