Open AccessVascular effects of a heme oxygenase inhibitor are enhanced in the absence of nitric oxide
Author(s) -
Fruzsina K. Johnson,
Federico J. Teran,
Minolfa C. PrietoCarrasquero,
Robert A. Johnson
Publication year - 2002
Publication title -
american journal of hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.009
H-Index - 136
eISSN - 1941-7225
pISSN - 0895-7061
DOI - 10.1016/s0895-7061(02)03062-5
Subject(s) - vasoconstriction , heme oxygenase , nitric oxide , vasodilation , endothelium , vascular smooth muscle , medicine , endocrinology , phenylephrine , heme , blood vessel , omega n methylarginine , sodium nitroprusside , hindlimb , nitric oxide synthase , pharmacology , chemistry , biochemistry , blood pressure , enzyme , smooth muscle
Vascular endothelium and smooth muscle express heme oxygenase (HO) that metabolizes heme to biliverdin, iron and carbon monoxide (CO). Carbon monoxide promotes endothelium-independent vasodilation, but also inhibits nitric oxide formation. This study examines the hypothesis that an inhibitor of HO promotes endothelium-independent vasoconstriction, which is attenuated in the presence of unabated nitric oxide formation.