Role of nitric oxide in vascular hyper-responsiveness to norepinephrine inhypertensive Dahl rats

Objective To determine whether the abnormal vascular responses observed in salt-sensitive hypertension are caused by an impairment in vascular nitric oxide function. Design Isometric tension was measured in aortic rings isola ted from Dahl salt-sensitive and salt-resistant rats fed a regular-salt (0. 4% NaCl) or a high-salt (8% NaCl) diet, with and without inhibition of endo genous nitric oxide synthesis. Methods and results Systolic arterial pressure, measured weekly by the tail -cuff method, increased markedly in DS rats with a high-salt diet but did n ot increase in the other groups, In aortic rings, norepinephrine evoked dos e-dependent contractions which were significantly increased in rings from D S rats with a high-salt diet, Pretreatment with N-omega-nitro-L-arginine me thyl ester (L-NAME), a nitric oxide synthase inhibitor, increased the norep inephrine-induced contraction in all groups and abolished differences in co ntractile responses between high-salt DS rats and the other groups. Acetylc holine induced endothelium-dependent relaxation, which was significantly de pressed in high-salt DS rats, L-NAME attenuated the acetylcholine-induced r elaxation in all groups and abolished the difference in relaxation response between high-salt DS rats and the other groups. Sodium nitroprusside-induc ed relaxation was significantly depressed in high-salt DS rats. Conclusions Vascular hypercontractile responses to norepinephrine in DS hyp ertensive rats can, in part, be explained by an impairment in endothelial n itric oxide production, J Hypertens 1998, 16:1611-1618 (C) Lippincott Willi ams & Wilkins.