Hypoxic pulmonary vasoconstriction is enhanced by inhibition of the synthesis of an endothelium derived relaxing factor

Stephen L. Archer; Jonathan P. Tolins; Leopoldo Raij; E. Kenneth Weir

doi:10.1016/0006-291X(89)91796-8

Hypoxic pulmonary vasoconstriction is enhanced by inhibition of the synthesis of an endothelium derived relaxing factor

Stephen L. Archer, Jonathan P. Tolins, Leopoldo Raij, E. Kenneth Weir

Physiology

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Abstract

Inhibition of the synthesis of endothelium derived relaxing factor by N^G-monomethyl-L-arginine, a competitive inhibitor of the synthesis of nitric oxide from L-arginine, enhances hypoxic pulmonary vasoconstriction in pulmonary artery rings and isolated, Krebs albumin perfused rat lungs. L-arginine rapidly reduces hypoxic vasoconstriction, particularly in lungs treated with N^G-monomethyl-L-arginine. Following administration of N^G-monomethyl-L-arginine, bradykinin-induced vasodilation is inhibited (p<0.01) and a bradykinin-induced vasoconstriction develops (p<0.001). N^G-monomethyl-L-arginine does not significantly diminish acetylcholine-induced vasodilatation in the isolated lung. N^G-monomethyl-L-arginine causes an endothelium-dependent vasoconstriction in pulmonary artery rings.

Original language	English (US)
Pages (from-to)	1198-1205
Number of pages	8
Journal	Biochemical and Biophysical Research Communications
Volume	164
Issue number	3
DOIs	https://doi.org/10.1016/0006-291X(89)91796-8
State	Published - Nov 15 1989

Bibliographical note

Funding Information:
This work was supported by the Veterans Administration.

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title = "Hypoxic pulmonary vasoconstriction is enhanced by inhibition of the synthesis of an endothelium derived relaxing factor",

abstract = "Inhibition of the synthesis of endothelium derived relaxing factor by NG-monomethyl-L-arginine, a competitive inhibitor of the synthesis of nitric oxide from L-arginine, enhances hypoxic pulmonary vasoconstriction in pulmonary artery rings and isolated, Krebs albumin perfused rat lungs. L-arginine rapidly reduces hypoxic vasoconstriction, particularly in lungs treated with NG-monomethyl-L-arginine. Following administration of NG-monomethyl-L-arginine, bradykinin-induced vasodilation is inhibited (p<0.01) and a bradykinin-induced vasoconstriction develops (p<0.001). NG-monomethyl-L-arginine does not significantly diminish acetylcholine-induced vasodilatation in the isolated lung. NG-monomethyl-L-arginine causes an endothelium-dependent vasoconstriction in pulmonary artery rings.",

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AU - Archer, Stephen L.

AU - Tolins, Jonathan P.

AU - Raij, Leopoldo

AU - Weir, E. Kenneth

N1 - Funding Information: This work was supported by the Veterans Administration.

PY - 1989/11/15

Y1 - 1989/11/15

N2 - Inhibition of the synthesis of endothelium derived relaxing factor by NG-monomethyl-L-arginine, a competitive inhibitor of the synthesis of nitric oxide from L-arginine, enhances hypoxic pulmonary vasoconstriction in pulmonary artery rings and isolated, Krebs albumin perfused rat lungs. L-arginine rapidly reduces hypoxic vasoconstriction, particularly in lungs treated with NG-monomethyl-L-arginine. Following administration of NG-monomethyl-L-arginine, bradykinin-induced vasodilation is inhibited (p<0.01) and a bradykinin-induced vasoconstriction develops (p<0.001). NG-monomethyl-L-arginine does not significantly diminish acetylcholine-induced vasodilatation in the isolated lung. NG-monomethyl-L-arginine causes an endothelium-dependent vasoconstriction in pulmonary artery rings.

AB - Inhibition of the synthesis of endothelium derived relaxing factor by NG-monomethyl-L-arginine, a competitive inhibitor of the synthesis of nitric oxide from L-arginine, enhances hypoxic pulmonary vasoconstriction in pulmonary artery rings and isolated, Krebs albumin perfused rat lungs. L-arginine rapidly reduces hypoxic vasoconstriction, particularly in lungs treated with NG-monomethyl-L-arginine. Following administration of NG-monomethyl-L-arginine, bradykinin-induced vasodilation is inhibited (p<0.01) and a bradykinin-induced vasoconstriction develops (p<0.001). NG-monomethyl-L-arginine does not significantly diminish acetylcholine-induced vasodilatation in the isolated lung. NG-monomethyl-L-arginine causes an endothelium-dependent vasoconstriction in pulmonary artery rings.

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Hypoxic pulmonary vasoconstriction is enhanced by inhibition of the synthesis of an endothelium derived relaxing factor

Abstract

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