Enhanced nitric oxide synthesis reverses salt-induced alterations in blood flow and cGMP levels

To understand the role of nitric oxide in salt-induced hypertension, we evaluated cardiovascular, hemodynamic and biochemical parameters in Dahl salt-sensitive rats fed low (0.3%) and high (8.0%) sodium diets. Two high salt groups received 1.25 and 2.5 g/L 1-arginine in their drinking water. After three weeks of treatment, blood pressure was greater in the high salt groups. 1-arginine did not modify salt-induced hypertension. Eicosapentaenoic acid (EPA) caused a smaller depressor response compared to normotensive rats. The increase in blood pressure was associated with decreases in aortic and renal blood flows. In renal artery, the reduction was counteracted by both 1-arginine doses; whereas in the aorta, only the higher 1-arginine one restored blood flow. The salt-induced reduction in aortic cyclic GMP level was only overcome by the higher 1-arginine treatment. These data suggest that at the dose levels tested, nitric oxide reverses the reduction in cGMP and blood flow, but not the blood pressure changes associated with salt-induced hypertension.