Hypertension, Vol 19, 290-295, Copyright © 1992 by American Heart Association
MA Boegehold
The aim of this study was to evaluate the influence of endogenous nitric
oxide on resting microvascular tone in the Dahl salt-sensitive (DS) rat and
to determine how this influence is altered in salt-induced hypertension.
Intravital microscopy was used to examine the arteriolar network in the
spinotrapezius muscle of DS rats maintained on low (0.45% NaCl) or high (4%
NaCl) salt diets for 6-7 weeks. Mean arterial pressure for DS rats on high
salt (163 +/- 3 mm Hg) was significantly greater than that for DS rats on
low salt (128 +/- 4 mm Hg). Inhibition of microvascular nitric oxide
synthesis with NG-nitro-L-arginine-methyl ester caused arteriolar
constriction in normotensive DS but not in hypertensive DS rats.
Application of L-arginine consistently caused arteriolar dilation in
normotensive DS but not hypertensive DS rats. In contrast, arteriolar
responses to iontophoretically applied acetylcholine and sodium
nitroprusside were similar in both groups. These results indicate that
basal release of nitric oxide, presumably from the endothelium, normally
influences arteriolar tone in skeletal muscle of DS rats and that this
influence is suppressed in established salt-induced hypertension. However,
the normal arteriolar response to acetylcholine in hypertensive DS rats
suggests that a generalized impairment of endothelial function may not
occur in the microcirculation of these animals. Unaltered arteriolar
responsiveness to sodium nitroprusside in hypertensive DS rats also
suggests that salt- induced hypertension is not accompanied by a change in
the responsiveness of arteriolar smooth muscle to nitric oxide.
ARTICLES
Reduced influence of nitric oxide on arteriolar tone in hypertensive Dahl rats
Department of Medicine, West Virginia University School of Medicine, Morgantown.
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