Reduced influence of nitric oxide on arteriolar tone in hypertensive Dahl rats.

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.