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

Research output: Contribution to journalArticlepeer-review

171 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1198-1205
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume164
Issue number3
DOIs
StatePublished - Nov 15 1989

Bibliographical note

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

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