Hypertension, Vol 19, 442-445, Copyright © 1992 by American Heart Association
W Auch-Schwelk, ZS Katusic and PM Vanhoutte
Acetylcholine evokes the simultaneous release of endothelium-derived
relaxing and contracting factors in aortas from spontaneously hypertensive
rats. Only relaxing factors are released in aortas from normotensive
controls. Experiments were designed to determine whether inhibitors of
endothelium-dependent relaxations modify endothelium- dependent
contractions. Rings of thoracic aortas of normotensive and spontaneously
hypertensive rats, with and without endothelium, were suspended in organ
chambers for isometric tension recording. Oxyhemoglobin (a scavenger of
endothelium-derived relaxing factor) and NG-monomethyl L-arginine (an
inhibitor of nitric oxide formation) augmented the contractions to
acetylcholine. Methylene blue (an inhibitor of soluble guanylate cyclase)
and superoxide dismutase (a scavenger of superoxide anions) did not modify
these contractions. The contractions in the presence of oxyhemoglobin or
NG-monomethyl L- arginine, like those in untreated rings, were
endothelium-dependent; they only occurred in aortas from spontaneously
hypertensive rats and were abolished by indomethacin. The contractions to
acetylcholine in the presence of oxyhemoglobin were not affected by
superoxide dismutase or deferoxamine. These data suggest that
endothelium-derived relaxing factor inhibits endothelium-dependent
contractions to acetylcholine in the spontaneously hypertensive rat aorta,
probably by chemical inactivation of the endothelium-derived contracting
factor rather than by stimulation of guanylate cyclase or scavenging of
oxygen-derived free radicals.
ARTICLES
Nitric oxide inactivates endothelium-derived contracting factor in the rat aorta
Mayo Clinic, Mayo Foundation, Department of Physiology and Biophysics, Rochester, Minn.
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